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2. Ferroptosis in health and disease.

Author

Berndt, Carsten, Alborzinia, Hamed, Amen, Vera, Ayton, Scott, Barayeu, Uladzimir, Bartelt, Alexander, Bayir, Hülya, Bebber, Christina, Birsoy, Kivanc, Böttcher, Jan, Brabletz, Simone, Brabletz, Thomas, Brown, Ashley, Brüne, Bernhard, Bulli, Giorgia, Bruneau, Alix, Chen, Quan, DeNicola, Gina, Dick, Tobias, Distéfano, Ayelén, Dixon, Scott, Engler, Jan, Esser-von Bieren, Julia, Fedorova, Maria, Friedmann Angeli, José, Friese, Manuel, Fuhrmann, Dominic, García-Sáez, Ana, Garbowicz, Karolina, Götz, Magdalena, Gu, Wei, Hammerich, Linda, Hassannia, Behrouz, Jiang, Xuejun, Jeridi, Aicha, Kang, Yun, Kagan, Valerian, Konrad, David, Kotschi, Stefan, Lei, Peng, Le Tertre, Marlène, Lev, Sima, Liang, Deguang, Linkermann, Andreas, Lohr, Carolin, Lorenz, Svenja, Luedde, Tom, Methner, Axel, Michalke, Bernhard, Milton, Anna, Min, Junxia, Mishima, Eikan, Müller, Sebastian, Motohashi, Hozumi, Muckenthaler, Martina, Murakami, Shohei, Olzmann, James, Pagnussat, Gabriela, Pan, Zijan, Papagiannakopoulos, Thales, Pedrera Puentes, Lohans, Pratt, Derek, Proneth, Bettina, Ramsauer, Lukas, Rodriguez, Raphael, Saito, Yoshiro, Schmidt, Felix, Schmitt, Carina, Schulze, Almut, Schwab, Annemarie, Schwantes, Anna, Soula, Mariluz, Spitzlberger, Benedikt, Stockwell, Brent, Thewes, Leonie, Thorn-Seshold, Oliver, Toyokuni, Shinya, Tonnus, Wulf, Trumpp, Andreas, Vandenabeele, Peter, Vanden Berghe, Tom, Venkataramani, Vivek, Vogel, Felix, von Karstedt, Silvia, Wang, Fudi, Westermann, Frank, Wientjens, Chantal, Wilhelm, Christoph, Wölk, Michele, Wu, Katherine, Yang, Xin, Yu, Fan, Zou, Yilong, and Conrad, Marcus

Subjects
Cancer, Cell death, Iron, Ischemia/reperfusion, Lipid peroxidation, Neurodegeneration
Abstract

Ferroptosis is a pervasive non-apoptotic form of cell death highly relevant in various degenerative diseases and malignancies. The hallmark of ferroptosis is uncontrolled and overwhelming peroxidation of polyunsaturated fatty acids contained in membrane phospholipids, which eventually leads to rupture of the plasma membrane. Ferroptosis is unique in that it is essentially a spontaneous, uncatalyzed chemical process based on perturbed iron and redox homeostasis contributing to the cell death process, but that it is nonetheless modulated by many metabolic nodes that impinge on the cells susceptibility to ferroptosis. Among the various nodes affecting ferroptosis sensitivity, several have emerged as promising candidates for pharmacological intervention, rendering ferroptosis-related proteins attractive targets for the treatment of numerous currently incurable diseases. Herein, the current members of a Germany-wide research consortium focusing on ferroptosis research, as well as key external experts in ferroptosis who have made seminal contributions to this rapidly growing and exciting field of research, have gathered to provide a comprehensive, state-of-the-art review on ferroptosis. Specific topics include: basic mechanisms, in vivo relevance, specialized methodologies, chemical and pharmacological tools, and the potential contribution of ferroptosis to disease etiopathology and progression. We hope that this article will not only provide established scientists and newcomers to the field with an overview of the multiple facets of ferroptosis, but also encourage additional efforts to characterize further molecular pathways modulating ferroptosis, with the ultimate goal to develop novel pharmacotherapies to tackle the various diseases associated with - or caused by - ferroptosis.

Published
2024

6. Seratrodast inhibits ferroptosis by suppressing lipid peroxidation

Author

Juliane Tschuck, Wulf Tonnus, Shubhangi Gavali, Andrea Kolak, Melodie Mallais, Francesca Maremonti, Mami Sato, Ina Rothenaigner, José Pedro Friedmann Angeli, Derek A. Pratt, Andreas Linkermann, and Kamyar Hadian

Subjects
Cytology, QH573-671
Abstract

Abstract Ferroptosis is a regulated and non-apoptotic form of cell death mediated by iron-dependent peroxidation of polyunsaturated fatty acyl tails in phospholipids. Research of the past years has shed light on the occurrence of ferroptosis in organ injury and degenerative diseases of the brain, kidney, heart, and other tissues. Hence, ferroptosis inhibition may prove therapeutically beneficial to treat distinct diseases. In this study, we explored the ferroptosis-modulating activity of seratrodast, an inhibitor of thromboxane A2 (TXA2) receptor, which is approved in some countries for the treatment of asthma. Interestingly, seratrodast suppressed ferroptosis, but not apoptosis and necroptosis; thus, demonstrating selective anti-ferroptotic activity. While seratrodast itself does not inhibit lipid peroxidation, it exhibits potent radical-trapping antioxidant activity upon reduction to its corresponding hydroquinone form—analogously to ubiquinone and vitamin K. Importantly, seratrodast ameliorated the severity of renal ischemia-reperfusion injury in mice. Together, this study provides a drug repurposing case, where seratrodast—a marketed drug—can undergo fast-forward preclinical/clinical development for the inhibition of ferroptosis in distinct degenerative diseases.

Published
2024
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7. Ferroptosis in health and disease

Author

Carsten Berndt, Hamed Alborzinia, Vera Skafar Amen, Scott Ayton, Uladzimir Barayeu, Alexander Bartelt, Hülya Bayir, Christina M. Bebber, Kivanc Birsoy, Jan P. Böttcher, Simone Brabletz, Thomas Brabletz, Ashley R. Brown, Bernhard Brüne, Giorgia Bulli, Alix Bruneau, Quan Chen, Gina M. DeNicola, Tobias P. Dick, Ayelén Distéfano, Scott J. Dixon, Jan B. Engler, Julia Esser-von Bieren, Maria Fedorova, José Pedro Friedmann Angeli, Manuel A. Friese, Dominic C. Fuhrmann, Ana J. García-Sáez, Karolina Garbowicz, Magdalena Götz, Wei Gu, Linda Hammerich, Behrouz Hassannia, Xuejun Jiang, Aicha Jeridi, Yun Pyo Kang, Valerian E. Kagan, David B. Konrad, Stefan Kotschi, Peng Lei, Marlène Le Tertre, Sima Lev, Deguang Liang, Andreas Linkermann, Carolin Lohr, Svenja Lorenz, Tom Luedde, Axel Methner, Bernhard Michalke, Anna V. Milton, Junxia Min, Eikan Mishima, Sebastian Müller, Hozumi Motohashi, Martina U. Muckenthaler, Shohei Murakami, James A. Olzmann, Gabriela Pagnussat, Zijan Pan, Thales Papagiannakopoulos, Lohans Pedrera Puentes, Derek A. Pratt, Bettina Proneth, Lukas Ramsauer, Raphael Rodriguez, Yoshiro Saito, Felix Schmidt, Carina Schmitt, Almut Schulze, Annemarie Schwab, Anna Schwantes, Mariluz Soula, Benedikt Spitzlberger, Brent R. Stockwell, Leonie Thewes, Oliver Thorn-Seshold, Shinya Toyokuni, Wulf Tonnus, Andreas Trumpp, Peter Vandenabeele, Tom Vanden Berghe, Vivek Venkataramani, Felix C.E. Vogel, Silvia von Karstedt, Fudi Wang, Frank Westermann, Chantal Wientjens, Christoph Wilhelm, Michele Wölk, Katherine Wu, Xin Yang, Fan Yu, Yilong Zou, and Marcus Conrad

Subjects
Cell death, Lipid peroxidation, Iron, Ischemia/reperfusion, Cancer, Neurodegeneration, Medicine (General), R5-920, Biology (General), QH301-705.5
Abstract

Ferroptosis is a pervasive non-apoptotic form of cell death highly relevant in various degenerative diseases and malignancies. The hallmark of ferroptosis is uncontrolled and overwhelming peroxidation of polyunsaturated fatty acids contained in membrane phospholipids, which eventually leads to rupture of the plasma membrane. Ferroptosis is unique in that it is essentially a spontaneous, uncatalyzed chemical process based on perturbed iron and redox homeostasis contributing to the cell death process, but that it is nonetheless modulated by many metabolic nodes that impinge on the cells’ susceptibility to ferroptosis. Among the various nodes affecting ferroptosis sensitivity, several have emerged as promising candidates for pharmacological intervention, rendering ferroptosis-related proteins attractive targets for the treatment of numerous currently incurable diseases. Herein, the current members of a Germany-wide research consortium focusing on ferroptosis research, as well as key external experts in ferroptosis who have made seminal contributions to this rapidly growing and exciting field of research, have gathered to provide a comprehensive, state-of-the-art review on ferroptosis. Specific topics include: basic mechanisms, in vivo relevance, specialized methodologies, chemical and pharmacological tools, and the potential contribution of ferroptosis to disease etiopathology and progression. We hope that this article will not only provide established scientists and newcomers to the field with an overview of the multiple facets of ferroptosis, but also encourage additional efforts to characterize further molecular pathways modulating ferroptosis, with the ultimate goal to develop novel pharmacotherapies to tackle the various diseases associated with – or caused by – ferroptosis.

Published
2024
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9. Protocol for isolating murine kidney tubules and ex vivo cell death assays

Author

Alexia Belavgeni, Francesca Maremonti, and Andreas Linkermann

Subjects
Cell Biology, Health Sciences, Molecular Biology, Science (General), Q1-390
Abstract

Summary: Isolating kidney tubules offers insights into their biological function without stroma, vascular cells, and immune system interference. Our murine tubule isolation protocol focuses on ex vivo cell death assays. We describe steps for solution preparation; kidney extraction, decapsulation, and slicing; and tubule isolation. We also outline assays like western blotting, lactate dehydrogenase release assay, and live-cell imaging of vital dyes during experimental acute tubular necrosis. This adaptable protocol allows the generation of outgrown primary tubular cells that maintain the features of tubular cells. : Publisher’s note: Undertaking any experimental protocol requires adherence to local institutional guidelines for laboratory safety and ethics.

Published
2024
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10. Gasdermin D drives focal crystalline thrombotic microangiopathy by accelerating immunothrombosis and necroinflammation

Author

Watanabe-Kusunoki, Kanako, Li, Chenyu, Bandeira Honda, Tâmisa Seeko, Zhao, Danyang, Kusunoki, Yoshihiro, Ku, John, Long, Hao, Klaus, Martin, Han, Chao, Braun, Attila, Mammadova-Bach, Elmina, Linkermann, Andreas, Van Avondt, Kristof, Richter, Mathis, Soehnlein, Oliver, Linder, Monika I., Klein, Christoph, Steiger, Stefanie, and Anders, Hans-Joachim

Published
2024
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11. Metformin potentiates nephrotoxicity by promoting NETosis in response to renal ferroptosis

Author

Zhaoxian Cai, Xiaotian Wu, Zijun Song, Shumin Sun, Yunxing Su, Tianyi Wang, Xihao Cheng, Yingying Yu, Chao Yu, En Chen, Wenteng Chen, Yongping Yu, Andreas Linkermann, Junxia Min, and Fudi Wang

Subjects
Cytology, QH573-671
Abstract

Abstract Given the rapidly aging population, aging-related diseases are becoming an excessive burden on the global healthcare system. Metformin has been shown to be beneficial to many age-related disorders, as well as increase lifespan in preclinical animal models. During the aging process, kidney function progressively declines. Currently, whether and how metformin protects the kidney remains unclear. In this study, among longevity drugs, including metformin, nicotinamide, resveratrol, rapamycin, and senolytics, we unexpectedly found that metformin, even at low doses, exacerbated experimentally-induced acute kidney injury (AKI) and increased mortality in mice. By single-cell transcriptomics analysis, we found that death of renal parenchymal cells together with an expansion of neutrophils occurs upon metformin treatment after AKI. We identified programmed cell death by ferroptosis in renal parenchymal cells and blocking ferroptosis, or depleting neutrophils protects against metformin-induced nephrotoxicity. Mechanistically, upon induction of AKI, ferroptosis in renal parenchymal cells initiates the migration of neutrophils to the site of injury via the surface receptor CXCR4–bound to metformin–iron–NGAL complex, which results in NETosis aggravated AKI. Finally, we demonstrated that reducing iron showed protective effects on kidney injury, which supports the notion that iron plays an important role in metformin-triggered AKI. Taken together, these findings delineate a novel mechanism underlying metformin-aggravated nephropathy and highlight the mechanistic relationship between iron, ferroptosis, and NETosis in the resulting AKI.

Published
2023
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13. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A., Abrams, John M., Adam, Dieter, Agostini, Massimiliano, Agostinis, Patrizia, Alnemri, Emad S., Altucci, Lucia, Amelio, Ivano, Andrews, David W., Aqeilan, Rami I., Arama, Eli, Baehrecke, Eric H., Balachandran, Siddharth, Bano, Daniele, Barlev, Nickolai A., Bartek, Jiri, Bazan, Nicolas G., Becker, Christoph, Bernassola, Francesca, Bertrand, Mathieu J. M., Bianchi, Marco E., Blagosklonny, Mikhail V., Blander, J. Magarian, Blandino, Giovanni, Blomgren, Klas, Borner, Christoph, Bortner, Carl D., Bove, Pierluigi, Boya, Patricia, Brenner, Catherine, Broz, Petr, Brunner, Thomas, Damgaard, Rune Busk, Calin, George A., Campanella, Michelangelo, Candi, Eleonora, Carbone, Michele, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K. -M., Chen, Guo-Qiang, Chen, Quan, Chen, Youhai H., Cheng, Emily H., Chipuk, Jerry E., Cidlowski, John A., Ciechanover, Aaron, Ciliberto, Gennaro, Conrad, Marcus, Cubillos-Ruiz, Juan R., Czabotar, Peter E., D’Angiolella, Vincenzo, Daugaard, Mads, Dawson, Ted M., Dawson, Valina L., De Maria, Ruggero, De Strooper, Bart, Debatin, Klaus-Michael, Deberardinis, Ralph J., Degterev, Alexei, Del Sal, Giannino, Deshmukh, Mohanish, Di Virgilio, Francesco, Diederich, Marc, Dixon, Scott J., Dynlacht, Brian D., El-Deiry, Wafik S., Elrod, John W., Engeland, Kurt, Fimia, Gian Maria, Galassi, Claudia, Ganini, Carlo, Garcia-Saez, Ana J., Garg, Abhishek D., Garrido, Carmen, Gavathiotis, Evripidis, Gerlic, Motti, Ghosh, Sourav, Green, Douglas R., Greene, Lloyd A., Gronemeyer, Hinrich, Häcker, Georg, Hajnóczky, György, Hardwick, J. Marie, Haupt, Ygal, He, Sudan, Heery, David M., Hengartner, Michael O., Hetz, Claudio, Hildeman, David A., Ichijo, Hidenori, Inoue, Satoshi, Jäättelä, Marja, Janic, Ana, Joseph, Bertrand, Jost, Philipp J., Kanneganti, Thirumala-Devi, Karin, Michael, Kashkar, Hamid, Kaufmann, Thomas, Kelly, Gemma L., Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Kluck, Ruth, Krysko, Dmitri V., Kulms, Dagmar, Kumar, Sharad, Lavandero, Sergio, Lavrik, Inna N., Lemasters, John J., Liccardi, Gianmaria, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., López-Otín, Carlos, Luedde, Tom, MacFarlane, Marion, Madeo, Frank, Malorni, Walter, Manic, Gwenola, Mantovani, Roberto, Marchi, Saverio, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Mastroberardino, Pier G., Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Gerry, Melino, Sonia, Miao, Edward A., Moll, Ute M., Muñoz-Pinedo, Cristina, Murphy, Daniel J., Niklison-Chirou, Maria Victoria, Novelli, Flavia, Núñez, Gabriel, Oberst, Andrew, Ofengeim, Dimitry, Opferman, Joseph T., Oren, Moshe, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pentimalli, Francesca, Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Pinton, Paolo, Porta, Giovanni, Prehn, Jochen H. M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rajalingam, Krishnaraj, Ravichandran, Kodi S., Rehm, Markus, Ricci, Jean-Ehrland, Rizzuto, Rosario, Robinson, Nirmal, Rodrigues, Cecilia M. P., Rotblat, Barak, Rothlin, Carla V., Rubinsztein, David C., Rudel, Thomas, Rufini, Alessandro, Ryan, Kevin M., Sarosiek, Kristopher A., Sawa, Akira, Sayan, Emre, Schroder, Kate, Scorrano, Luca, Sesti, Federico, Shao, Feng, Shi, Yufang, Sica, Giuseppe S., Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stephanou, Anastasis, Stockwell, Brent R., Strapazzon, Flavie, Strasser, Andreas, Sun, Liming, Sun, Erwei, Sun, Qiang, Szabadkai, Gyorgy, Tait, Stephen W. G., Tang, Daolin, Tavernarakis, Nektarios, Troy, Carol M., Turk, Boris, Urbano, Nicoletta, Vandenabeele, Peter, Vanden Berghe, Tom, Vander Heiden, Matthew G., Vanderluit, Jacqueline L., Verkhratsky, Alexei, Villunger, Andreas, von Karstedt, Silvia, Voss, Anne K., Vousden, Karen H., Vucic, Domagoj, Vuri, Daniela, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ruoning, Wang, Ying, Weber, Achim, Wood, Will, Yamazaki, Takahiro, Yang, Huang-Tian, Zakeri, Zahra, Zawacka-Pankau, Joanna E., Zhang, Lin, Zhang, Haibing, Zhivotovsky, Boris, Zhou, Wenzhao, Piacentini, Mauro, Kroemer, Guido, and Galluzzi, Lorenzo

Published
2023
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14. High RIPK3 expression is associated with a higher risk of early kidney transplant failure

Author

Wahida, Adam, Schmaderer, Christoph, Büttner-Herold, Maike, Branca, Caterina, Donakonda, Sainitin, Haberfellner, Flora, Torrez, Carlos, Schmitz, Jessica, Schulze, Tobias, Seibt, Tobias, Öllinger, Rupert, Engleitner, Thomas, Haller, Bernhard, Steiger, Katja, Günthner, Roman, Lorenz, Georg, Yabal, Monica, Bachmann, Quirin, Braunisch, Matthias C., Moog, Philipp, Matevossian, Edouard, Aßfalg, Volker, Thorban, Stefan, Renders, Lutz, Späth, Martin R., Müller, Roman-Ulrich, Stippel, Dirk L., Weichert, Wilko, Slotta-Huspenina, Julia, von Vietinghoff, Sibylle, Viklicky, Ondrej, Green, Douglas R., Rad, Roland, Amann, Kerstin, Linkermann, Andreas, Bräsen, Jan Hinrich, Heemann, Uwe, and Kemmner, Stephan

Published
2023
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15. Mechanisms and clinical relevance of the bidirectional relationship of viral infections with metabolic diseases

Author

Perakakis, Nikolaos, Harb, Hani, Hale, Benjamin G, Varga, Zsuzsanna, Steenblock, Charlotte, Kanczkowski, Waldemar, Alexaki, Vasileia Ismini, Ludwig, Barbara, Mirtschink, Peter, Solimena, Michele, Toepfner, Nicole, Zeissig, Sebastian, Gado, Manuel, Abela, Irene Alma, Beuschlein, Felix, Spinas, Giatgen A, Cavelti-Weder, Claudia, Gerber, Philipp A, Huber, Michael, Trkola, Alexandra, Puhan, Milo A, Wong, Wendy Wei-Lynn, Linkermann, Andreas, Mohan, Viswanathan, Lehnert, Hendrik, Nawroth, Peter, Chavakis, Triantafyllos, Mingrone, Geltrude, Wolfrum, Christian, Zinkernagel, Annelies S, and Bornstein, Stefan R

Published
2023
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17. List Of Contributors

Author

Abraham, Roshini Sarah, primary, Afzali, Behdad, additional, Águeda, Ana, additional, Akin, Cem, additional, Albanesi, Cristina, additional, Antiochos, Brendan, additional, Aranow, Cynthia, additional, Atkinson, John P., additional, Aune, Thomas M., additional, Babu, Subash, additional, Balko, Justin, additional, Ballow, Mark, additional, Bean, Rachel, additional, Belavgeni, Alexia, additional, Berek, Claudia, additional, Beukelman, Timothy, additional, Beziat, Vivien, additional, Bimler, Lynn, additional, Andrew Bird, J., additional, Blutt, Sarah E., additional, Boguniewicz, Mark, additional, Boisson, Bertrand, additional, Boisson-Dupuis, Stéphanie, additional, Borzova, Elena, additional, Bottazzi, Maria, additional, Boyaka, Prosper N., additional, Bridges, John, additional, Browne, Sarah K., additional, Burks, A. Wesley, additional, Bustamante, Jacinta, additional, Casanova, Jean-Laurent, additional, Chan, Alice, additional, Chan, Edwin S.L., additional, Chatham, Walter Winn, additional, Chinen, Javier, additional, Christopher-Stine, Lisa, additional, Coates, Emily, additional, Cope, Andrew P., additional, Corry, David B., additional, Cosme, Joana, additional, Cron, Randy Q., additional, Dalakas, Marinos C., additional, Dann, Sara M., additional, Das, Satya, additional, Daughety, Molly M., additional, Diamond, Betty, additional, Dispenzieri, Angela, additional, Durham, Stephen R., additional, Eagar, Todd N., additional, Al-Hosni, Michelle, additional, Elitzur, Sarah, additional, Elmets, Craig A., additional, Erkan, Doruk, additional, Fleisher, Thomas A., additional, Fonacier, Luz, additional, Fontenot, Andrew P., additional, Fragoulis, George, additional, Francischetti, Ivo M.B., additional, Freiwald, Tilo, additional, Frew, Anthony J., additional, Fujihashi, Kohtaro, additional, Gadina, Massimo, additional, Gapin, Laurent, additional, Gatt, Moshe E., additional, Gershwin, M. Eric, additional, Gillespie, Susan L., additional, Gordon, Lynn K., additional, Goronzy, Jörg J., additional, Grattan, Clive E., additional, Greenspan, Neil S., additional, Gschwend, Anna, additional, Gustafson, Claire E., additional, Hackett, Tillie-Louise, additional, Hamilton, Robert G., additional, Happe, Myra, additional, Harrison, Leonard C., additional, Helbling, Arthur, additional, Heckmann, Emmaline, additional, Hogquist, Kristin, additional, Hohl, Tobias M., additional, Holland, Steven M., additional, Hotez, Peter J., additional, Houser, Katherine, additional, Huntingdon, Nicholas D., additional, Hwangpo, Tracy, additional, Izraeli, Shai, additional, Jaffe, Elaine S., additional, Jalkanen, Sirpa, additional, Java, Anuja, additional, Johnson, Douglas B., additional, Johnson, Tory, additional, Jordan, Michael B., additional, Joshi, Shyam R., additional, Jouanguy, Emmanuelle, additional, Kaminski, Henry J., additional, Kaufmann, Stefan H.E., additional, Khan, David A., additional, Kheradmand, Farrah, additional, Khokar, Dilawar Singh, additional, Khoury, Paneez, additional, Klein, Bruce S., additional, Klion, Amy D., additional, Kohn, Donald B., additional, Kono, Michihito, additional, Korngold, Robert, additional, Koulouri, Vasiliki, additional, Kuhns, Douglas B., additional, Kulkarni, Hrishikesh S., additional, Kuo, Caroline Y., additional, Kusner, Linda L., additional, Lahouti, Arash, additional, Lane, Laura C., additional, Laurence, Arian, additional, Lee, Joyce S., additional, Lee, S. Thera, additional, Leung, Donald Y.M., additional, Levy, Ofer, additional, Lewis, Dorothy E., additional, Li, Evan, additional, Libby, Peter, additional, Lichtman, Andrew H., additional, Linkermann, Andreas, additional, Lionakis, Michail S., additional, Liszewski, M. Kathryn, additional, Lockshin, Michael D., additional, Priel, Debra Long, additional, Lorenz, Adi Zoref, additional, Ludwig, Ralf J., additional, Luong, Amber, additional, Luqmani, Raashid Ahmed, additional, Mackay, Meggan, additional, Mahr, Alfred, additional, Malley, Tamir, additional, Mannon, Elinor C., additional, Mannon, Peter J., additional, Mannon, Roslyn B., additional, Manns, Michael P., additional, Maresso, Anthony, additional, Matson, Scott M., additional, Mavragani, Clio P., additional, Maynard, Craig L., additional, McDonald, Douglas, additional, Meylan, Françoise, additional, Miller, Stephen D., additional, Mitchell, Anna L., additional, Monos, Dimitri S., additional, Mueller, Scott N., additional, Mulders-Manders, Catharina M., additional, Munshi, Pashna N., additional, Murphy, Philip M., additional, Noel, Pierre, additional, Notarangelo, Luigi D., additional, Nunes-Santos, Cristiane J., additional, Nussbaum, Robert L., additional, Nutman, Thomas B., additional, Nutt, Stephen L., additional, O'Neill, Lorraine, additional, O'Shea, John J., additional, Ortel, Thomas L., additional, Pai, Sung-Yun, additional, Paul, Mary E., additional, Pearce, Simon, additional, Peterson, Erik J., additional, Pittaluga, Stefania, additional, Polverino, Francesca, additional, Puck, Jennifer M., additional, Puel, Anne, additional, Radbruch, Andreas, additional, Rajalingam, Raja, additional, Reece, Stephen T., additional, Reveille, John D., additional, Rich, Robert R., additional, Ridley, Lauren K., additional, Romeo, Andrew R., additional, Rooney, Cliona M., additional, Rosen, Antony, additional, Rosenzweig, Sergio, additional, Rouse, Barry T., additional, Rowley, Scott D., additional, Sahiner, Umit Murat, additional, Sakaguchi, Shimon, additional, Salinas, Whitney, additional, Salmi, Marko, additional, Satola, Sarah, additional, Schechter, Marcos, additional, Schmidt, Enno, additional, Schroeder, Harry W., additional, Schwartzberg, Pamela L., additional, Sciumè, Giuseppe, additional, Segal, Benjamin M., additional, Selmi, Carlo, additional, Sharabi, Amir, additional, Shimano, Kristin Ammon, additional, Sikorski, Patricia M., additional, Simon, Anna, additional, Smith, Gideon P., additional, Song, Joo Y., additional, Stephens, David S., additional, Stephens, Robin, additional, Sun, Michel M., additional, Beretta-Piccoli, Benedetta Terziroli, additional, Tonnus, Wulf, additional, Torgerson, Troy R., additional, Torres, Raul Martin, additional, Treat, Jennifer D., additional, Tsokos, George C., additional, Uzel, Gülbü, additional, Uzonna, Jude E., additional, van der Hilst, Jeroen C.H., additional, van der Meer, Jos W.M., additional, Varga, John, additional, Waldman, Meryl, additional, Weatherhead, Jill, additional, Weiser, Peter, additional, Weyand, Cornelia M., additional, Wigley, Fredrick M., additional, Wing, James B., additional, Wood, Kathryn J., additional, Wilde, Shyra, additional, Xu, Hui, additional, Yusuf, Nabiha, additional, Zerbe, Christa S., additional, Zhang, Qian, additional, Ben-Yehuda, Dina, additional, Zhang, Shen-Ying, additional, and Zieske, Arthur W., additional

Published
2023
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19. Gasdermin D-deficient mice are hypersensitive to acute kidney injury

Author

Wulf Tonnus, Francesca Maremonti, Alexia Belavgeni, Markus Latk, Yoshihiro Kusunoki, Anne Brucker, Anne von Mässenhausen, Claudia Meyer, Sophie Locke, Florian Gembardt, Kristina Beer, Paul Hoppenz, Jan U. Becker, Christian Hugo, Hans-Joachim Anders, Stefan R. Bornstein, Feng Shao, and Andreas Linkermann

Subjects
Cytology, QH573-671
Abstract

Abstract Signaling pathways of regulated necrosis, such as necroptosis and ferroptosis, contribute to acute kidney injury (AKI), but the role of pyroptosis is unclear. Pyroptosis is mediated by the pore-forming protein gasdermin D (GSDMD). Here, we report a specific pattern of GSDMD-protein expression in the peritubular compartment of mice that underwent bilateral ischemia and reperfusion injury (IRI). Along similar lines, the GSDMD-protein expression in whole kidney lysates increased during the first 84 h following cisplatin-induced AKI. Importantly, unlike whole kidney lysates, no GSDMD-protein expression was detectable in isolated kidney tubules. In IRI and cisplatin-induced AKI, GSDMD-deficient mice exhibited hypersensitivity to injury as assessed by tubular damage, elevated markers of serum urea, and serum creatinine. This hypersensitivity was reversed by a combined deficiency of GSDMD and the necroptosis mediator mixed lineage kinase domain-like (MLKL). In conclusion, we demonstrate a non-cell autonomous role for GSDMD in protecting the tubular compartment from necroptosis-mediated damage in IRI.

Published
2022
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21. A non-canonical vitamin K cycle is a potent ferroptosis suppressor

Author

Mishima, Eikan, Ito, Junya, Wu, Zijun, Nakamura, Toshitaka, Wahida, Adam, Doll, Sebastian, Tonnus, Wulf, Nepachalovich, Palina, Eggenhofer, Elke, Aldrovandi, Maceler, Henkelmann, Bernhard, Yamada, Ken-ichi, Wanninger, Jonas, Zilka, Omkar, Sato, Emiko, Feederle, Regina, Hass, Daniela, Maida, Adriano, Mourão, André Santos Dias, Linkermann, Andreas, Geissler, Edward K., Nakagawa, Kiyotaka, Abe, Takaaki, Fedorova, Maria, Proneth, Bettina, Pratt, Derek A., and Conrad, Marcus

Published
2022
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22. Rubicon-deficiency sensitizes mice to mixed lineage kinase domain-like (MLKL)-mediated kidney ischemia-reperfusion injury

Author

Wulf Tonnus, Sophie Locke, Claudia Meyer, Francesca Maremonti, Lena Eggert, Anne von Mässenhausen, Stefan R. Bornstein, Douglas R. Green, and Andreas Linkermann

Subjects
Cytology, QH573-671
Abstract

Abstract The cytosolic protein rubicon (RUBCN) has been implicated in the removal of necrotic debris and autoimmunity. However, the role of RUBCN in models of acute kidney injury (AKI), a condition that typically involves necrotic kidney tubules, was not investigated. Here, we demonstrate that RUBCN-deficient mice are hypersensitive to renal damage induced by ischemia-reperfusion injury (IRI) and cisplatin-induced AKI. Combined deficiency of RUBCN and mixed lineage kinase domain-like (MLKL) partially reversed the sensitivity in the IRI model suggesting that the absence of RUBCN sensitizes to necroptosis in that model. Necroptosis is known to contribute to TNFα-induced severe inflammatory response syndrome (SIRS), but we detected no statistically significant difference in overall survival following injection of TNFα in RUBCN-deficient mice. We additionally generated RUBCN-deficient mice which lack gasdermin D (GSDMD), the terminal mediator of pyroptosis, but no reversal of the AKI phenotype was observed. Finally, and in contrast to the previous understanding of the role of RUBCN, we did not find a significant autoimmune phenotype in RUBCN-deficient mice, but detected chronic kidney injury (CKD) in aged RUBCN-deficient mice of both sexes. In summary, our data indicate that RUBCN-deficient mice are hypersensitive to kidney injury.

Published
2022
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23. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018

Author

Galluzzi, Lorenzo, Vitale, Ilio, Aaronson, Stuart A, Abrams, John M, Adam, Dieter, Agostinis, Patrizia, Alnemri, Emad S, Altucci, Lucia, Amelio, Ivano, Andrews, David W, Annicchiarico-Petruzzelli, Margherita, Antonov, Alexey V, Arama, Eli, Baehrecke, Eric H, Barlev, Nickolai A, Bazan, Nicolas G, Bernassola, Francesca, Bertrand, Mathieu JM, Bianchi, Katiuscia, Blagosklonny, Mikhail V, Blomgren, Klas, Borner, Christoph, Boya, Patricia, Brenner, Catherine, Campanella, Michelangelo, Candi, Eleonora, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K-M, Chandel, Navdeep S, Cheng, Emily H, Chipuk, Jerry E, Cidlowski, John A, Ciechanover, Aaron, Cohen, Gerald M, Conrad, Marcus, Cubillos-Ruiz, Juan R, Czabotar, Peter E, D’Angiolella, Vincenzo, Dawson, Ted M, Dawson, Valina L, De Laurenzi, Vincenzo, De Maria, Ruggero, Debatin, Klaus-Michael, DeBerardinis, Ralph J, Deshmukh, Mohanish, Di Daniele, Nicola, Di Virgilio, Francesco, Dixit, Vishva M, Dixon, Scott J, Duckett, Colin S, Dynlacht, Brian D, El-Deiry, Wafik S, Elrod, John W, Fimia, Gian Maria, Fulda, Simone, García-Sáez, Ana J, Garg, Abhishek D, Garrido, Carmen, Gavathiotis, Evripidis, Golstein, Pierre, Gottlieb, Eyal, Green, Douglas R, Greene, Lloyd A, Gronemeyer, Hinrich, Gross, Atan, Hajnoczky, Gyorgy, Hardwick, J Marie, Harris, Isaac S, Hengartner, Michael O, Hetz, Claudio, Ichijo, Hidenori, Jäättelä, Marja, Joseph, Bertrand, Jost, Philipp J, Juin, Philippe P, Kaiser, William J, Karin, Michael, Kaufmann, Thomas, Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N, Klionsky, Daniel J, Knight, Richard A, Kumar, Sharad, Lee, Sam W, Lemasters, John J, Levine, Beth, Linkermann, Andreas, Lipton, Stuart A, Lockshin, Richard A, López-Otín, Carlos, Lowe, Scott W, Luedde, Tom, Lugli, Enrico, MacFarlane, Marion, Madeo, Frank, Malewicz, Michal, Malorni, Walter, and Manic, Gwenola

Subjects
Biochemistry and Cell Biology, Biological Sciences, Animals, Cell Death, Humans, Lysosomes, Mitochondrial Membrane Transport Proteins, Mitochondrial Permeability Transition Pore, Necrosis, Medical and Health Sciences, Biochemistry & Molecular Biology, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field.

Published
2018

25. Targeting ferroptosis protects against experimental (multi)organ dysfunction and death

Author

Van Coillie, Samya, Van San, Emily, Goetschalckx, Ines, Wiernicki, Bartosz, Mukhopadhyay, Banibrata, Tonnus, Wulf, Choi, Sze Men, Roelandt, Ria, Dumitrascu, Catalina, Lamberts, Ludwig, Dams, Geert, Weyts, Wannes, Huysentruyt, Jelle, Hassannia, Behrouz, Ingold, Irina, Lele, Suhas, Meyer, Evelyne, Berg, Maya, Seurinck, Ruth, Saeys, Yvan, Vermeulen, An, van Nuijs, Alexander L. N., Conrad, Marcus, Linkermann, Andreas, Rajapurkar, Mohan, Vandenabeele, Peter, Hoste, Eric, Augustyns, Koen, and Vanden Berghe, Tom

Published
2022
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28. COVID-19 and metabolic disease: mechanisms and clinical management

Author

Steenblock, Charlotte, Schwarz, Peter E H, Ludwig, Barbara, Linkermann, Andreas, Zimmet, Paul, Kulebyakin, Konstantin, Tkachuk, Vsevolod A, Markov, Alexander G, Lehnert, Hendrik, de Angelis, Martin Hrabě, Rietzsch, Hannes, Rodionov, Roman N, Khunti, Kamlesh, Hopkins, David, Birkenfeld, Andreas L, Boehm, Bernhard, Holt, Richard I G, Skyler, Jay S, DeVries, J Hans, Renard, Eric, Eckel, Robert H, Alberti, K George M M, Geloneze, Bruno, Chan, Juliana C, Mbanya, Jean Claude, Onyegbutulem, Henry C, Ramachandran, Ambady, Basit, Abdul, Hassanein, Mohamed, Bewick, Gavin, Spinas, Giatgen A, Beuschlein, Felix, Landgraf, Rüdiger, Rubino, Francesco, Mingrone, Geltrude, and Bornstein, Stefan R

Published
2021
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29. A single genetic locus controls both expression of DPEP1/CHMP1A and kidney disease development via ferroptosis

Author

Yuting Guan, Xiujie Liang, Ziyuan Ma, Hailong Hu, Hongbo Liu, Zhen Miao, Andreas Linkermann, Jacklyn N. Hellwege, Benjamin F. Voight, and Katalin Susztak

Subjects
Science
Abstract

Identifying causal variants and genes is an essential step in interpreting GWAS loci. Here, the authors investigate a kidney disease GWAS locus with functional genomics data, CRISPR editing and mouse experiments to identify DPEP1 and CHMP1A as putative kidney disease genes via ferroptosis.

Published
2021
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30. Dysfunction of the key ferroptosis-surveilling systems hypersensitizes mice to tubular necrosis during acute kidney injury

Author

Wulf Tonnus, Claudia Meyer, Christian Steinebach, Alexia Belavgeni, Anne von Mässenhausen, Nadia Zamora Gonzalez, Francesca Maremonti, Florian Gembardt, Nina Himmerkus, Markus Latk, Sophie Locke, Julian Marschner, Wenjun Li, Spencer Short, Sebastian Doll, Irina Ingold, Bettina Proneth, Christoph Daniel, Nazanin Kabgani, Rafael Kramann, Stephen Motika, Paul J. Hergenrother, Stefan R. Bornstein, Christian Hugo, Jan Ulrich Becker, Kerstin Amann, Hans-Joachim Anders, Daniel Kreisel, Derek Pratt, Michael Gütschow, Marcus Conrad, and Andreas Linkermann

Subjects
Science
Abstract

Necroptosis, a form of cell death, occurs in acute renal injury. Here, the authors show that ferroptosis—a form of cell death dependent on iron - also occurs during acute kidney injury, and show that an inhibitor of ferroptosis can improve survival in a mouse model of acute kidney damage.

Published
2021
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31. Viral infiltration of pancreatic islets in patients with COVID-19

Author

Charlotte Steenblock, Stefanie Richter, Ilona Berger, Marko Barovic, Janine Schmid, Undine Schubert, Natalia Jarzebska, Anne von Mässenhausen, Andreas Linkermann, Annette Schürmann, Jessica Pablik, Thomas Dienemann, Katja Evert, Roman N. Rodionov, Natalia Y. Semenova, Vsevolod A. Zinserling, Raul R. Gainetdinov, Gustavo Baretton, Dirk Lindemann, Michele Solimena, Barbara Ludwig, and Stefan R. Bornstein

Subjects
Science
Abstract

New-onset hyperglycemia and complications of preexisting diabetes have been observed in COVID-19 patients, however, the underlying mechanisms are not fully understood. Here, the authors show that SARS-CoV-2 is detectable in both endocrine and exocrine cells of the pancreata of patients with COVID-19.

Published
2021
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32. Beyond the Paradigm: Novel Functions of Renin-Producing Cells

Author

Steglich, Anne, Hickmann, Linda, Linkermann, Andreas, Bornstein, Stefan, Hugo, Christian, Todorov, Vladimir T., Pedersen, Stine Helene Falsig, Editor-in-Chief, Cordat, Emmanuelle, Series Editor, Barber, Diane, Series Editor, Leipziger, Jens, Series Editor, Pardo, Luis A., Series Editor, Stock, Christian, Series Editor, Schmitt, Nicole, Series Editor, and O'Donnell, Martha E., Series Editor

Published
2020
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34. The biology of ferroptosis in kidney disease.

Author

Seibt, Tobias, Wahida, Adam, Hoeft, Konrad, Kemmner, Stephan, Linkermann, Andreas, Mishima, Eikan, and Conrad, Marcus

Subjects
BILAYER lipid membranes, ACUTE kidney failure, CELL membranes, MEMBRANE lipids, LIPID metabolism, CELL death, LIPID peroxidation (Biology)
Abstract

Ferroptosis is a regulated cell death modality triggered by iron-dependent lipid peroxidation. Ferroptosis plays a causal role in the pathophysiology of various diseases, making it a promising therapeutic target. Unlike all other cell death modalities dependent on distinct signaling cues, ferroptosis occurs when cellular antioxidative defense mechanisms fail to suppress the oxidative destruction of cellular membranes, eventually leading to cell membrane rupture. Physiologically, only two such surveillance systems are known to efficiently prevent the lipid peroxidation chain reaction by reducing (phospho)lipid hydroperoxides to their corresponding alcohols or by reducing radicals in phospholipid bilayers, thus maintaining the integrity of lipid membranes. Mechanistically, these two systems are linked to the reducing capacity of glutathione peroxidase 4 (GPX4) by consuming glutathione (GSH) on one hand and ferroptosis suppressor protein 1 (FSP1, formerly AIFM2) on the other. Notably, the importance of ferroptosis suppression in physiological contexts has been linked to a particular vulnerability of renal tissue. In fact, early work has shown that mice genetically lacking Gpx4 rapidly succumb to acute renal failure with pathohistological features of acute tubular necrosis. Promising research attempting to implicate ferroptosis in various renal disease entities, particularly those with proximal tubular involvement, has generated a wealth of knowledge with widespread potential for clinical translation. Here, we provide a brief overview of the involvement of ferroptosis in nephrology. Our goal is to introduce this expanding field for clinically versed nephrologists in the hope of spurring future efforts to prevent ferroptosis in the pathophysiological processes of the kidney. [ABSTRACT FROM AUTHOR]

Published
2024
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36. Tissue inflammation induced by constitutively active STING is mediated by enhanced TNF signaling

Author

Luksch, Hella, primary, Schulze, Felix, additional, Geißler-Lösch, David, additional, Sprott, David, additional, Höfs, Lennart, additional, Szegö, Eva M, additional, Tonnus, Wulf, additional, Winkler, Stefan, additional, Günther, Claudia, additional, Linkermann, Andreas, additional, Behrendt, Rayk, additional, Teichmann, Lino L, additional, Falkenburger, Björn H, additional, and Rösen-Wolff, Angela, additional

Published
2024
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37. Ferroptosis Biology

Author

Seibt, Tobias, primary, Wahida, Adam, additional, Hoeft, Konrad, additional, Kemmner, Stephan, additional, Linkermann, Andreas, additional, Mishima, Eikan, additional, and Conrad, Marcus, additional

Published
2024
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38. Treatment with siRNAs is commonly associated with GPX4 up-regulation and target knockdown-independent sensitization to ferroptosis

Author

von Mässenhausen, Anne, primary, Schlecht, Marlena Nastassja, additional, Beer, Kristina, additional, Maremonti, Francesca, additional, Tonnus, Wulf, additional, Belavgeni, Alexia, additional, Gavali, Shubhangi, additional, Flade, Karolin, additional, Riley, Joel S., additional, Zamora Gonzalez, Nadia, additional, Brucker, Anne, additional, Becker, Jorunn Naila, additional, Tmava, Mirela, additional, Meyer, Claudia, additional, Peitzsch, Mirko, additional, Hugo, Christian, additional, Gembardt, Florian, additional, Angeli, Jose Pedro Friedmann, additional, Bornstein, Stefan R., additional, Tait, Stephen W. G., additional, and Linkermann, Andreas, additional

Published
2024
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39. International consensus guidelines for the definition, detection, and interpretation of autophagy-dependent ferroptosis

Author

Chen, Xin, primary, Tsvetkov, Andrey S., additional, Shen, Han-Ming, additional, Isidoro, Ciro, additional, Ktistakis, Nicholas T., additional, Linkermann, Andreas, additional, Koopman, Werner J.H., additional, Simon, Hans-Uwe, additional, Galluzzi, Lorenzo, additional, Luo, Shouqing, additional, Xu, Daqian, additional, Gu, Wei, additional, Peulen, Olivier, additional, Cai, Qian, additional, Rubinsztein, David C., additional, Chi, Jen-Tsan, additional, Zhang, Donna D., additional, Li, Changfeng, additional, Toyokuni, Shinya, additional, Liu, Jinbao, additional, Roh, Jong-Lyel, additional, Dai, Enyong, additional, Juhasz, Gabor, additional, Liu, Wei, additional, Zhang, Jianhua, additional, Yang, Minghua, additional, Liu, Jiao, additional, Zhu, Ling-Qiang, additional, Zou, Weiping, additional, Piacentini, Mauro, additional, Ding, Wen-Xing, additional, Yue, Zhenyu, additional, Xie, Yangchun, additional, Petersen, Morten, additional, Gewirtz, David A., additional, Mandell, Michael A., additional, Chu, Charleen T., additional, Sinha, Debasish, additional, Eftekharpour, Eftekhar, additional, Zhivotovsky, Boris, additional, Besteiro, Sébastien, additional, Gabrilovich, Dmitry I., additional, Kim, Do-Hyung, additional, Kagan, Valerian E., additional, Bayir, Hülya, additional, Chen, Guang-Chao, additional, Ayton, Scott, additional, Lünemann, Jan D., additional, Komatsu, Masaaki, additional, Krautwald, Stefan, additional, Loos, Ben, additional, Baehrecke, Eric H., additional, Wang, Jiayi, additional, Lane, Jon D., additional, Sadoshima, Junichi, additional, Yang, Wan Seok, additional, Gao, Minghui, additional, Münz, Christian, additional, Thumm, Michael, additional, Kampmann, Martin, additional, Yu, Di, additional, Lipinski, Marta M., additional, Jones, Jace W., additional, Jiang, Xuejun, additional, Zeh, Herbert J., additional, Kang, Rui, additional, Klionsky, Daniel J., additional, Kroemer, Guido, additional, and Tang, Daolin, additional

Published
2024
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40. Exquisite sensitivity of adrenocortical carcinomas to induction of ferroptosis

Author

Belavgeni, Alexia, Bornstein, Stefan R., von Mässenhausen, Anne, Tonnus, Wulf, Stumpf, Julian, Meyer, Claudia, Othmar, Evelyn, Latk, Markus, Kanczkowski, Waldemar, Kroiss, Matthias, Hantel, Constanze, Hugo, Christian, Fassnacht, Martin, Ziegler, Christian G., Schally, Andrew V., Krone, Nils P., and Linkermann, Andreas

Published
2019

42. International consensus guidelines for the definition, detection, and interpretation of autophagy-dependent ferroptosis

Author

Chen, Xin, Tsvetkov, Andrey S., Shen, Han-ming, Isidoro, Ciro, Ktistakis, Nicholas T., Linkermann, Andreas, Koopman, Werner J.h., Simon, Hans-uwe, Galluzzi, Lorenzo, Luo, Shouqing, Xu, Daqian, Gu, Wei, Peulen, Olivier, Cai, Qian, Rubinsztein, David C., Chi, Jen-tsan, Zhang, Donna D., Li, Changfeng, Toyokuni, Shinya, Liu, Jinbao, Roh, Jong-lyel, Dai, Enyong, Juhasz, Gabor, Liu, Wei, Zhang, Jianhua, Yang, Minghua, Liu, Jiao, Zhu, Ling-qiang, Zou, Weiping, Piacentini, Mauro, Ding, Wen-xing, Yue, Zhenyu, Xie, Yangchun, Petersen, Morten, Gewirtz, David A., Mandell, Michael A., Chu, Charleen T., Sinha, Debasish, Eftekharpour, Eftekhar, Zhivotovsky, Boris, Besteiro, Sébastien, Gabrilovich, Dmitry I., Kim, Do-hyung, Kagan, Valerian E., Bayir, Hülya, Chen, Guang-chao, Ayton, Scott, Lünemann, Jan D., Komatsu, Masaaki, Krautwald, Stefan, Loos, Ben, Baehrecke, Eric H., Wang, Jiayi, Lane, Jon D., Sadoshima, Junichi, Yang, Wan Seok, Gao, Minghui, Münz, Christian, Thumm, Michael, Kampmann, Martin, Yu, Di, Lipinski, Marta M., Jones, Jace W., Jiang, Xuejun, Zeh, Herbert J., Kang, Rui, Klionsky, Daniel J., Kroemer, Guido, Tang, Daolin, Chen, Xin, Tsvetkov, Andrey S., Shen, Han-ming, Isidoro, Ciro, Ktistakis, Nicholas T., Linkermann, Andreas, Koopman, Werner J.h., Simon, Hans-uwe, Galluzzi, Lorenzo, Luo, Shouqing, Xu, Daqian, Gu, Wei, Peulen, Olivier, Cai, Qian, Rubinsztein, David C., Chi, Jen-tsan, Zhang, Donna D., Li, Changfeng, Toyokuni, Shinya, Liu, Jinbao, Roh, Jong-lyel, Dai, Enyong, Juhasz, Gabor, Liu, Wei, Zhang, Jianhua, Yang, Minghua, Liu, Jiao, Zhu, Ling-qiang, Zou, Weiping, Piacentini, Mauro, Ding, Wen-xing, Yue, Zhenyu, Xie, Yangchun, Petersen, Morten, Gewirtz, David A., Mandell, Michael A., Chu, Charleen T., Sinha, Debasish, Eftekharpour, Eftekhar, Zhivotovsky, Boris, Besteiro, Sébastien, Gabrilovich, Dmitry I., Kim, Do-hyung, Kagan, Valerian E., Bayir, Hülya, Chen, Guang-chao, Ayton, Scott, Lünemann, Jan D., Komatsu, Masaaki, Krautwald, Stefan, Loos, Ben, Baehrecke, Eric H., Wang, Jiayi, Lane, Jon D., Sadoshima, Junichi, Yang, Wan Seok, Gao, Minghui, Münz, Christian, Thumm, Michael, Kampmann, Martin, Yu, Di, Lipinski, Marta M., Jones, Jace W., Jiang, Xuejun, Zeh, Herbert J., Kang, Rui, Klionsky, Daniel J., Kroemer, Guido, and Tang, Daolin

Abstract

Macroautophagy/autophagy is a complex degradation process with a dual role in cell death that is influenced by the cell types that are involved and the stressors they are exposed to. Ferroptosis is an iron-dependent oxidative form of cell death characterized by unrestricted lipid peroxidation in the context of heterogeneous and plastic mechanisms. Recent studies have shed light on the involvement of specific types of autophagy (e.g. ferritinophagy, lipophagy, and clockophagy) in initiating or executing ferroptotic cell death through the selective degradation of anti-injury proteins or organelles. Conversely, other forms of selective autophagy (e.g. reticulophagy and lysophagy) enhance the cellular defense against ferroptotic damage. Dysregulated autophagy-dependent ferroptosis has implications for a diverse range of pathological conditions. This review aims to present an updated definition of autophagy-dependent ferroptosis, discuss influential substrates and receptors, outline experimental methods, and propose guidelines for interpreting the results., Macroautophagy/autophagy is a complex degradation process with a dual role in cell death that is influenced by the cell types that are involved and the stressors they are exposed to. Ferroptosis is an iron-dependent oxidative form of cell death characterized by unrestricted lipid peroxidation in the context of heterogeneous and plastic mechanisms. Recent studies have shed light on the involvement of specific types of autophagy (e.g. ferritinophagy, lipophagy, and clockophagy) in initiating or executing ferroptotic cell death through the selective degradation of anti-injury proteins or organelles. Conversely, other forms of selective autophagy (e.g. reticulophagy and lysophagy) enhance the cellular defense against ferroptotic damage. Dysregulated autophagy-dependent ferroptosis has implications for a diverse range of pathological conditions. This review aims to present an updated definition of autophagy-dependent ferroptosis, discuss influential substrates and receptors, outline experimental methods, and propose guidelines for interpreting the results. Abbreviation: 3-MA:3-methyladenine; 4HNE: 4-hydroxynonenal; ACD: accidentalcell death; ADF: autophagy-dependentferroptosis; ARE: antioxidant response element; BH2:dihydrobiopterin; BH4: tetrahydrobiopterin; BMDMs: bonemarrow-derived macrophages; CMA: chaperone-mediated autophagy; CQ:chloroquine; DAMPs: danger/damage-associated molecular patterns; EMT,epithelial-mesenchymal transition; EPR: electronparamagnetic resonance; ER, endoplasmic reticulum; FRET: Försterresonance energy transfer; GFP: green fluorescent protein;GSH: glutathione;IF: immunofluorescence; IHC: immunohistochemistry; IOP, intraocularpressure; IRI: ischemia-reperfusion injury; LAA: linoleamide alkyne;MDA: malondialdehyde; PGSK: Phen Green™ SK;RCD: regulatedcell death; PUFAs: polyunsaturated fatty acids; RFP: red fluorescentprotein;ROS: reactive oxygen species; TBA: thiobarbituricacid; TBARS: thiobarbituric acid reactive substances; TEM:transmis

Published
2024

43. Ferroptosis in health and disease

Author

Berndt, C, Alborzinia, H, Amen, VS, Ayton, S, Barayeu, U, Bartelt, A, Bayir, H, Bebber, CM, Birsoy, K, Bottcher, JP, Brabletz, S, Brabletz, T, Brown, AR, Bruene, B, Bulli, G, Bruneau, A, Chen, Q, DeNicola, GM, Dick, TP, Distefano, A, Dixon, SJ, Engler, JB, Esser-von Bieren, J, Fedorova, M, Angeli, JPF, Friese, MA, Fuhrmann, DC, Garcia-Saez, AJ, Garbowicz, K, Gotz, M, Gu, W, Hammerich, L, Hassannia, B, Jiang, X, Jeridi, A, Kang, YP, Kagan, VE, Konrad, DB, Kotschi, S, Lei, P, Le Tertre, M, Lev, S, Liang, D, Linkermann, A, Lohr, C, Lorenz, S, Luedde, T, Methner, A, Michalke, B, Milton, A, Min, J, Mishima, E, Mueller, S, Motohashi, H, Muckenthaler, MU, Murakami, S, Olzmann, JA, Pagnussat, G, Pan, Z, Papagiannakopoulos, T, Puentes, LP, Pratt, DA, Proneth, B, Ramsauer, L, Rodriguez, R, Saito, Y, Schmidt, F, Schmitt, C, Schulze, A, Schwab, A, Schwantes, A, Soula, M, Spitzlberger, B, Stockwell, BR, Thewes, L, Thorn-Seshold, O, Toyokuni, S, Tonnus, W, Trumpp, A, Vandenabeele, P, Vanden Berghe, T, Venkataramani, V, Vogel, FCE, von Karstedt, S, Wang, F, Westermann, F, Wientjens, C, Wilhelm, C, Wolk, M, Wu, K, Yang, X, Yu, F, Zou, Y, Conrad, M, Berndt, C, Alborzinia, H, Amen, VS, Ayton, S, Barayeu, U, Bartelt, A, Bayir, H, Bebber, CM, Birsoy, K, Bottcher, JP, Brabletz, S, Brabletz, T, Brown, AR, Bruene, B, Bulli, G, Bruneau, A, Chen, Q, DeNicola, GM, Dick, TP, Distefano, A, Dixon, SJ, Engler, JB, Esser-von Bieren, J, Fedorova, M, Angeli, JPF, Friese, MA, Fuhrmann, DC, Garcia-Saez, AJ, Garbowicz, K, Gotz, M, Gu, W, Hammerich, L, Hassannia, B, Jiang, X, Jeridi, A, Kang, YP, Kagan, VE, Konrad, DB, Kotschi, S, Lei, P, Le Tertre, M, Lev, S, Liang, D, Linkermann, A, Lohr, C, Lorenz, S, Luedde, T, Methner, A, Michalke, B, Milton, A, Min, J, Mishima, E, Mueller, S, Motohashi, H, Muckenthaler, MU, Murakami, S, Olzmann, JA, Pagnussat, G, Pan, Z, Papagiannakopoulos, T, Puentes, LP, Pratt, DA, Proneth, B, Ramsauer, L, Rodriguez, R, Saito, Y, Schmidt, F, Schmitt, C, Schulze, A, Schwab, A, Schwantes, A, Soula, M, Spitzlberger, B, Stockwell, BR, Thewes, L, Thorn-Seshold, O, Toyokuni, S, Tonnus, W, Trumpp, A, Vandenabeele, P, Vanden Berghe, T, Venkataramani, V, Vogel, FCE, von Karstedt, S, Wang, F, Westermann, F, Wientjens, C, Wilhelm, C, Wolk, M, Wu, K, Yang, X, Yu, F, Zou, Y, and Conrad, M

Abstract

Ferroptosis is a pervasive non-apoptotic form of cell death highly relevant in various degenerative diseases and malignancies. The hallmark of ferroptosis is uncontrolled and overwhelming peroxidation of polyunsaturated fatty acids contained in membrane phospholipids, which eventually leads to rupture of the plasma membrane. Ferroptosis is unique in that it is essentially a spontaneous, uncatalyzed chemical process based on perturbed iron and redox homeostasis contributing to the cell death process, but that it is nonetheless modulated by many metabolic nodes that impinge on the cells' susceptibility to ferroptosis. Among the various nodes affecting ferroptosis sensitivity, several have emerged as promising candidates for pharmacological intervention, rendering ferroptosis-related proteins attractive targets for the treatment of numerous currently incurable diseases. Herein, the current members of a Germany-wide research consortium focusing on ferroptosis research, as well as key external experts in ferroptosis who have made seminal contributions to this rapidly growing and exciting field of research, have gathered to provide a comprehensive, state-of-the-art review on ferroptosis. Specific topics include: basic mechanisms, in vivo relevance, specialized methodologies, chemical and pharmacological tools, and the potential contribution of ferroptosis to disease etiopathology and progression. We hope that this article will not only provide established scientists and newcomers to the field with an overview of the multiple facets of ferroptosis, but also encourage additional efforts to characterize further molecular pathways modulating ferroptosis, with the ultimate goal to develop novel pharmacotherapies to tackle the various diseases associated with - or caused by - ferroptosis.

Published
2024

44. Efficacy of finerenone in patients with type 2 diabetes, chronic kidney disease and altered markers of liver steatosis and fibrosis: A FIDELITY subgroup analysis

Author

Perakakis, Nikolaos; https://orcid.org/0000-0002-2319-6603, Bornstein, Stefan R; https://orcid.org/0000-0002-5211-2536, Birkenfeld, Andreas L; https://orcid.org/0000-0003-1407-9023, Linkermann, Andreas; https://orcid.org/0000-0001-6287-9725, Demir, Münevver, Anker, Stefan D, Filippatos, Gerasimos; https://orcid.org/0000-0002-5640-0332, Pitt, Bertram, Rossing, Peter; https://orcid.org/0000-0002-1531-4294, Ruilope, Luis M, Kolkhof, Peter, Lawatscheck, Robert, Scott, Charlie, Bakris, George L; https://orcid.org/0000-0003-1183-1267, FIDELIO-DKD and FIGARO-DKD investigators, Perakakis, Nikolaos; https://orcid.org/0000-0002-2319-6603, Bornstein, Stefan R; https://orcid.org/0000-0002-5211-2536, Birkenfeld, Andreas L; https://orcid.org/0000-0003-1407-9023, Linkermann, Andreas; https://orcid.org/0000-0001-6287-9725, Demir, Münevver, Anker, Stefan D, Filippatos, Gerasimos; https://orcid.org/0000-0002-5640-0332, Pitt, Bertram, Rossing, Peter; https://orcid.org/0000-0002-1531-4294, Ruilope, Luis M, Kolkhof, Peter, Lawatscheck, Robert, Scott, Charlie, Bakris, George L; https://orcid.org/0000-0003-1183-1267, and FIDELIO-DKD and FIGARO-DKD investigators

Abstract

AIM Investigating the effect of finerenone on liver function, cardiovascular and kidney composite outcomes in patients with chronic kidney disease and type 2 diabetes, stratified by their risk of liver steatosis, inflammation and fibrosis. MATERIALS AND METHODS Post hoc analysis stratified patients (N = 13 026) by liver fibrosis and enzymes: high risk of steatosis (hepatic steatosis index >36); elevated transaminases [alanine transaminase (ALT) >33 (males) and >25 IU/L (females)]; and fibrosis-4 (FIB-4) index scores >3.25, >2.67 and >1.30. Liver enzymes were assessed by changes in ALT, aspartate aminotransferase and gamma-glutamyl transferase. Composite kidney outcome was defined as onset of kidney failure, sustained estimated glomerular filtration rate decline ≥57% from baseline over ≥4 weeks or kidney death. Composite cardiovascular outcome was defined as cardiovascular death, non-fatal myocardial infarction, non-fatal stroke or hospitalization for heart failure. RESULTS ALT, aspartate aminotransferase and gamma-glutamyl transferase levels were consistent between treatment groups and remained stable throughout. Finerenone consistently reduced the risk of composite kidney outcome, irrespective of altered liver tests. Higher FIB-4 score was associated with higher incidence rates of composite cardiovascular outcome. Finerenone reduced the risk of composite cardiovascular outcome versus placebo in FIB-4 subgroups by 52% (>3.25), 39% (>2.67) and 24% (>1.30) (p values for interaction = .01, .13 and .03, respectively). CONCLUSIONS Finerenone has neutral effects on liver parameters in patients with chronic kidney disease and type 2 diabetes. Finerenone showed robust and consistent kidney benefits in patients with altered liver tests, and profound cardiovascular benefits even in patients with higher FIB-4 scores who were at high risk of developing cardiovascular complications.

Published
2024

45. Efficacy of finerenone in patients with type 2 diabetes, chronic kidney disease and altered markers of liver steatosis and fibrosis:A FIDELITY subgroup analysis

Author

Perakakis, Nikolaos, Bornstein, Stefan R, Birkenfeld, Andreas L, Linkermann, Andreas, Demir, Münevver, Anker, Stefan D, Filippatos, Gerasimos, Pitt, Bertram, Rossing, Peter, Ruilope, Luis M, Kolkhof, Peter, Lawatscheck, Robert, Scott, Charlie, Bakris, George L, Perakakis, Nikolaos, Bornstein, Stefan R, Birkenfeld, Andreas L, Linkermann, Andreas, Demir, Münevver, Anker, Stefan D, Filippatos, Gerasimos, Pitt, Bertram, Rossing, Peter, Ruilope, Luis M, Kolkhof, Peter, Lawatscheck, Robert, Scott, Charlie, and Bakris, George L

Abstract

AIM: Investigating the effect of finerenone on liver function, cardiovascular and kidney composite outcomes in patients with chronic kidney disease and type 2 diabetes, stratified by their risk of liver steatosis, inflammation and fibrosis.MATERIALS AND METHODS: Post hoc analysis stratified patients (N = 13 026) by liver fibrosis and enzymes: high risk of steatosis (hepatic steatosis index >36); elevated transaminases [alanine transaminase (ALT) >33 (males) and >25 IU/L (females)]; and fibrosis-4 (FIB-4) index scores >3.25, >2.67 and >1.30. Liver enzymes were assessed by changes in ALT, aspartate aminotransferase and gamma-glutamyl transferase. Composite kidney outcome was defined as onset of kidney failure, sustained estimated glomerular filtration rate decline ≥57% from baseline over ≥4 weeks or kidney death. Composite cardiovascular outcome was defined as cardiovascular death, non-fatal myocardial infarction, non-fatal stroke or hospitalization for heart failure.RESULTS: ALT, aspartate aminotransferase and gamma-glutamyl transferase levels were consistent between treatment groups and remained stable throughout. Finerenone consistently reduced the risk of composite kidney outcome, irrespective of altered liver tests. Higher FIB-4 score was associated with higher incidence rates of composite cardiovascular outcome. Finerenone reduced the risk of composite cardiovascular outcome versus placebo in FIB-4 subgroups by 52% (>3.25), 39% (>2.67) and 24% (>1.30) (p values for interaction = .01, .13 and .03, respectively).CONCLUSIONS: Finerenone has neutral effects on liver parameters in patients with chronic kidney disease and type 2 diabetes. Finerenone showed robust and consistent kidney benefits in patients with altered liver tests, and profound cardiovascular benefits even in patients with higher FIB-4 scores who were at high risk of developing cardiovascular complications.

Published
2024

46. Musicality: A Game to Improve Musical Perception

Author

Khalass, Nouri, Zarnomitrou, Georgia, Haque, Kazi Injamamul, Salmi, Salim, Maulini, Simon, Linkermann, Tanja, Salamon, Nestor Z., Timothy Balint, J., Bidarra, Rafael, Hutchison, David, Series Editor, Kanade, Takeo, Series Editor, Kittler, Josef, Series Editor, Kleinberg, Jon M., Series Editor, Mattern, Friedemann, Series Editor, Mitchell, John C., Series Editor, Naor, Moni, Series Editor, Pandu Rangan, C., Series Editor, Steffen, Bernhard, Series Editor, Terzopoulos, Demetri, Series Editor, Tygar, Doug, Series Editor, Gentile, Manuel, editor, Allegra, Mario, editor, and Söbke, Heinrich, editor

Published
2019
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47. A guideline on the molecular ecosystem regulating ferroptosis

Author

Dai, Enyong, Chen, Xin, Linkermann, Andreas, Jiang, Xuejun, Kang, Rui, Kagan, Valerian E., Bayir, Hülya, Yang, Wan Seok, Garcia-Saez, Ana J., Ioannou, Maria S., Janowitz, Tobias, Ran, Qitao, Gu, Wei, Gan, Boyi, Krysko, Dmitri V., Zhu, Xiaofeng, Wang, Jiayi, Krautwald, Stefan, Toyokuni, Shinya, Xie, Yangchun, Greten, Florian R., Yi, Qing, Schick, Joel, Liu, Jiao, Gabrilovich, Dmitry I., Liu, Jinbao, Zeh, Herbert J., Zhang, Donna D., Yang, Minghua, Iovanna, Juan, Kopf, Manfred, Adolph, Timon E., Chi, Jen-Tsan, Li, Changfeng, Ichijo, Hidenori, Karin, Michael, Sankaran, Vijay G., Zou, Weiping, Galluzzi, Lorenzo, Bush, Ashley I., Li, Binghui, Melino, Gerry, Baehrecke, Eric H., Lotze, Michael T., Klionsky, Daniel J., Stockwell, Brent R., Kroemer, Guido, and Tang, Daolin

Abstract

Ferroptosis, an intricately regulated form of cell death characterized by uncontrolled lipid peroxidation, has garnered substantial interest since this term was first coined in 2012. Recent years have witnessed remarkable progress in elucidating the detailed molecular mechanisms that govern ferroptosis induction and defence, with particular emphasis on the roles of heterogeneity and plasticity. In this Review, we discuss the molecular ecosystem of ferroptosis, with implications that may inform and enable safe and effective therapeutic strategies across a broad spectrum of diseases.

Published
2024
Full Text
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49. Apoptotic cell death in disease—Current understanding of the NCCD 2023

Author

Associazione Italiana per la Ricerca sul Cancro, Italian Institute for Genomic Medicine, Compagnia di San Paolo, Vitale, Ilio [0000-0002-5918-1841], Pietrocola, Federico [0000-0002-2930-234X], Guilbaud, Emma [0000-0001-5261-1944], Aaronson, Stuart A. [0000-0002-4643-0474], Dieter, Adam [0000-0002-5668-5032], Agostini, Massimiliano [0000-0003-3124-2072], Agostinis, Patrizia [0000-0003-1314-2115], Alnemri, Emad S. [0000-0002-7295-3383], Altucci, Lucia [0000-0002-7312-5387], Amelio, Ivano [0000-0002-9126-5391], Andrews, David W. [0000-0002-9266-7157], Aqeilan, Rami I. [0000-0002-6034-023X], Arama, Eli [0000-0001-5953-0629], Balachandran, Siddharth [0000-0003-2084-1803], Bano, Daniele [0000-0002-9617-5504], Bartek, Jiri [0000-0003-2013-7525], Bazan, Nicolas G. [0000-0002-9243-5444], Bernassola, Francesca [0000-0002-8883-8654], Bertrand, Mathieu J. M. [0000-0001-9000-0626], Bianchi, Marco Emilio [0000-0002-5329-6445], Blander, J. Magarian [0000-0001-9207-1700], Blandino, Giovanni [0000-0002-6970-2241], Blomgren, Klas [0000-0002-0476-7271], Bortner, Carl D. [0000-0002-5444-6628], Bove, Pierluigi [0000-0002-4788-2982], Boya, Patricia [0000-0003-3045-951X], Broz, Petr [0000-0002-2334-7790], Damgaard, Rune Busk [0000-0002-1709-6534], Calin, George A. [0000-0002-7427-0578], Campanella, Michelangelo [0000-0002-6948-4184], Candi, Eleonora [0000-0001-8332-4825], Carbone, Michele [0000-0001-8928-8474], Carmona-Gutierrez, Didac [0000-0001-7548-7771], Cecconi, Francesco [0000-0002-5614-4359], Chen, Guo‑Qiang [0000-0002-7226-1782], Cheng, Emily H. [0000-0002-3595-2648], Chipuk, Jerry E. [0000-0002-1337-842X], Cidlowski, John A. [0000-0003-1420-0516], Ciechanover, Aaron [0000-0001-9184-8944], Ciliberto, Gennaro [0000-0003-2851-8605], Conrad, Marcus [0000-0003-1140-5612], Czabotar, Peter E. [0000-0002-2594-496X], D’Angiolella, Vincenzo [0000-0001-8365-9094], Daugaard, Mads [0000-0001-8383-055X], Dawson, Valina L. [0000-0002-2915-3970], De Maria, Ruggero [0000-0003-2255-0583], Debatin, Klaus-Michael [0000-0002-8397-1886], Deberardinis, Ralph J. [0000-0002-2705-7432], Degterev, Alexei [0000-0002-8240-7132], Del Sal, Giannino [0000-0003-2185-6003], Deshmukh, Mohanish [0000-0002-2597-5862], Di Virgilio, Francesco [0000-0003-3566-1362], Diederich, Marc [0000-0003-0115-4725], Dixon, Scott J. [0000-0001-6230-8199], El-Deiry, Wafik S. [0000-0002-9577-8266], Elrod, John W. [0000-0003-3925-2224], Engeland, Kurt [0000-0003-3525-0440], Fimia, Gian María [0000-0003-4438-3325], Ganini, Carlo [0000-0002-5839-3965], García-Sáez, Ana J. [0000-0002-3894-5945], Garg, Abhishek D. [0000-0002-9976-9922], Garrido, Carmen [0000-0003-1368-1493], Gavathiotis, Evripidis [0000-0001-6319-8331], Ghosh, Sourav [0000-0001-5990-8708], Green, Douglas R. [0000-0002-7332-1417], Gronemeyer, Hinrich [0000-0001-9454-2449}, Häcker, Georg [0000-0003-1058-5746], Hajnóczky, György [0000-0003-3813-2570], Hardwick, J. Marie [0000-0002-4847-2045], Haupt, Ygal [0000-0001-5925-0096], He, Sudan [0000-0002-0846-1210], Heery, David M. [0000-0002-5035-2392], Hengartner, Michael O. [0000-0002-7584-596X], Hetz, Claudio [0000-0003-1120-7966], Hildeman, David A. [0000-0002-0421-8483], Ichijo, Hidenori [0000-0002-5005-6438], Jäättelä, Marja [0000-0001-5950-7111], Janic, Ana [0000-0002-4200-2560], Joseph, Bertrand [0000-0001-5655-9979], Jost, Philipp J. [0000-0003-2454-0362], Kanneganti, Thirumala-Devi [0000-0002-6395-6443], Karin, Michael [0000-0002-2758-6473], Kashkar, Hamid [0000-0003-2796-1429], Kaufmann, Thomas [0000-0001-9906-874X], Kelly, Gemma L. [0000-0002-6533-1201], Kepp, Oliver [0000-0002-6081-9558], Kimchi, Adi [0000-0002-8236-8989], Klionsky, Daniel J. [0000-0002-7828-8118], Kluck, Ruth [0000-0002-7101-1925], Krysko, Dmitri V. [0000-0002-9692-2047], Kulms, Dagmar [0000-0001-6874-0548], Kumar, Sharad [0000-0001-7126-9814], Lavandero, Sergio [0000-0003-4258-1483], Lavrik, Inna N. [0000-0002-9324-309X], Liccardi, Gianmaria [0000-0002-2662-1281], Linkermann, Andreas [0000-0001-6287-9725], Lipton, Stuart A. [0000-0002-3490-1259], Lockshin, Richard A. [0000-0002-4389-4898], López-Otín, Carlos [0000-0001-6964-1904], Luedde, Tom [0000-0002-6288-8821], MacFarlane, Marion [0000-0001-7886-1159], Madeo, Frank [0000-0002-5070-1329], Malorni, Walter [0000-0002-1223-7000], Manic, Gwenola [0000-0003-3759-8029], Marchi, Saverio [0000-0003-2708-1843], Marine, Jean-Christophe [0000-0003-2433-9837], Martin, Seamus J. [0000-0002-8539-3143], Martinou, Jean-Claude [0000-0002-9847-2051], Mastroberardino, Pier G. [0000-0003-2364-4258], Medema, Jan Paul [0000-0003-3045-2924], Mehlen, Patrick [0000-0003-1743-5417], Meier, Pascal [0000-0003-2760-6523], Melino, Gerry [0000-0001-9428-5972], Melino, Sonia [0000-0001-7694-5279], Miao, Edward A. [0000-0001-7295-3490], Moll, Ute M. [0000-0003-1908-7516], Muñoz-Pinedo, Cristina [0000-0002-9120-664X], Murphy, Daniel J. [0000-0002-5538-5468], Niklison-Chirou, Maria Victoria [0000-0002-2147-370X], Novelli, Flavia [0000-0002-3746-7478], Oberst, Andrew [0000-0002-9500-7912], Ofengeim, Dimitry [0000-0003-2348-3642], Opferman, Joseph T. [0000-0002-1147-5621], Oren, Moshe [0000-0003-4311-7172], Pagano, Michele [0000-0003-3210-2442], Panaretakis, Theocharis [0000-0001-5754-6950], Pasparakis, Manolis [0000-0002-9870-0966], Penninger, Josef M. [0000-0002-8194-3777], Pentimalli, Francesca [0000-0003-4740-6801], Pereira, David M. [0000-0003-0384-7592], Pervaiz, Shazib [0000-0002-4738-019X], Peter, Marcus E. [0000-0003-3216-036X], Pinton, Paolo [0000-0001-7108-6508], Porta, Giovanni [0000-0001-5260-2415], Puthalakath, Hamsa [0000-0001-5178-1175], Rabinovich, Gabriel A. [0000-0002-0947-8735], Rajalingam, Krishnaraj [0000-0002-4175-9633], Ravinchandran, Kodi S. [0000-0001-9049-1410], Rehm, Markus [0000-0001-6149-9261], Ricci, Jean-Ehrland [0000-0003-1585-8117], Rizzuto, Rosario [0000-0001-7044-5097], Robinson, Nirmal [0000-0002-7361-9491], Rotblat, Barak [0000-0003-2985-7115], Rothlin, Carla V. [0000-0002-5693-5572], Rubinsztein, David C. [0000-0001-5002-5263], Rufini, Alessandro [0000-0002-5855-655X], Ryan, Kevin M. [0000-0002-1059-9681], Sarosiek, Kristopher A. [0000-0002-4618-5085], Sawa, Akira [0000-0003-1401-3008], Sayan, Emre [0000-0002-5291-1485], Schroder, Kate [0000-0001-9261-3805], Scorrano, Luca [0000-0002-8515-8928], Sesti, Federico [0000-0002-2761-9693], Shi, Yufang [0000-0001-8964-319X], Sica, Giuseppe [0000-0002-7407-0584], Silke, John [0000-0002-7611-5774], Simon, Hans-Uwe [0000-0002-9404-7736], Sistigu, Antonella [0000-0002-2528-1238], Stockwell, Brent R. [0000-0002-3532-3868], Strappazzon, Flavie [0000-0003-0285-7449], Sun, Liming [0000-0002-0136-5605], Sun, Erwei [0000-0001-5664-513X], Szabadkai, G [0000-0002-3006-3577], Tait, Stephen W. G. [0000-0001-7697-132X], Tang, Daolin [0000-0002-1903-6180], Tavernarakis, Nektarios [0000-0002-5253-1466], Turk, Boris [0000-0002-9007-5764], Urbano, Nicoletta [0000-0003-1822-155X], Vandenabeele, Peter [0000-0002-6669-8822], Vanden Berghe, Tom [0000-0002-1633-0974], Vander Heiden, Matthew G. [0000-0002-6702-4192], Vanderluit, Jacqueline L. [0000-0002-4960-920X], Verkhratsky, A. [0000-0003-2592-9898], Villunger, Andreas [0000-0001-8259-4153], Von Karstedt, Silvia [0000-0002-7816-5919], Voss, Anne K. [0000-0002-3853-9381], Vucic, Domagoj [0000-0003-3614-8093], Vuri, Daniela [0000-0001-8693-3845], Wagner, Erwin F. [0000-0001-7872-0196], Walczak, Henning [0000-0002-6312-4591], Wallach, David [0000-0003-2724-9757], Wang, Ruoning [0000-0001-9798-8032], Weber, Achim [0000-0003-0073-3637], Yamazaki, Takahiro [0000-0002-7420-4394], Zakeri, Zahra [0000-0003-4386-8072], Zawacka-Pankau, Joanna E. [0000-0002-7415-2942], Zhivotovsky, Boris [0000-0002-2238-3482], Piacentini, Mauro [0000-0003-2919-1296], Kroemer, Guido [0000-0002-9334-4405], Galluzzi, Lorenzo [0000-0003-2257-8500 ], Vitale, Ilio, Pietrocola, Federico, Guilbaud, Emma, Aaronson, Stuart A., Abrams, John M., Dieter, Adam, Agostini, Massimiliano, Agostinis, Patrizia, Alnemri, Emad S., Altucci, Lucia, Amelio, Ivano, Andrews, David W., Aqeilan, Rami I., Arama, Eli, Baehrecke, Eric H., Balachandran, Siddharth, Bano, Daniele, Barlev, Nickolai A., Bartek, Jiri, Bazan, Nicolas G., Becker, Christoph, Bernassola, Francesca, Bertrand, Mathieu J. M., Bianchi, Marco Emilio, Blagosklonny, Mikhail V., Blander, J. Magarian, Blandino, Giovanni, Blomgren, Klas, Bomer, Christoph, Bortner, Carl D., Bove, Pierluigi, Boya, Patricia, Brenner, Catherine, Broz, Petr, Brunner, T., Damgaard, Rune Busk, Calin, George A., Campanella, Michelangelo, Candi, Eleonora, Carbone, Michele, Carmona-Gutierrez, Didac, Cecconi, Francesco, Chan, Francis K.-M., Chen, Guo‑Qiang, Chen, Quan, Chen, Youhai H., Cheng, Emily H., Chipuk, Jerry E., Cidlowski, John A., Ciechanover, Aaron, Ciliberto, Gennaro, Conrad, Marcus, Cubillos-Ruiz, Juan R., Czabotar, Peter E., D’Angiolella, Vincenzo, Daugaard, Mads, Dawson, Ted M., Dawson, Valina L., De Maria, Ruggero, De Strooper, B., Debatin, Klaus-Michael, Deberardinis, Ralph J., Degterev, Alexei, Del Sal, Giannino, Deshmukh, Mohanish, Di Virgilio, Francesco, Diederich, Marc, Dixon, Scott J., Dynlacht, Brian D., El-Deiry, Wafik S., Elrod, John W., Engeland, Kurt, Fimia, Gian María, Galassi, Claudia, Ganini, Carlo, García-Sáez, Ana J., Garg, Abhishek D., Garrido, Carmen, Gavathiotis, Evripidis, Gerlic, Motti, Ghosh, Sourav, Green, Douglas R., Greene, Lloyd A., Gronemeyer, Hinrich, Häcker, Georg, Hajnóczky, György, Hardwick, J. Marie, Haupt, Ygal, He, Sudan, Heery, David M., Hengartner, Michael O., Hetz, Claudio, Hildeman, David A., Ichijo, Hidenori, Inoue, Satoshi, Jäättelä, Marja, Janic, Ana, Joseph, Bertrand, Jost, Philipp J., Kanneganti, Thirumala-Devi, Karin, Michael, Kashkar, Hamid, Kaufmann, Thomas, Kelly, Gemma L., Kepp, Oliver, Kimchi, Adi, Kitsis, Richard N., Klionsky, Daniel J., Kluck, Ruth, Krysko, Dmitri V., Kulms, Dagmar, Kumar, Sharad, Lavandero, Sergio, Lavrik, Inna N., Lemasters, John J., Liccardi, Gianmaria, Linkermann, Andreas, Lipton, Stuart A., Lockshin, Richard A., López-Otín, Carlos, Luedde, Tom, MacFarlane, Marion, Madeo, Frank, Malorni, Walter, Manic, Gwenola, Mantovani, Roberto, Marchi, Saverio, Marine, Jean-Christophe, Martin, Seamus J., Martinou, Jean-Claude, Mastroberardino, Pier G., Medema, Jan Paul, Mehlen, Patrick, Meier, Pascal, Melino, Gerry, Melino, Sonia, Miao, Edward A., Moll, Ute M., Muñoz-Pinedo, Cristina, Murphy, Daniel J., Niklison-Chirou, Maria Victoria, Novelli, Flavia, Núñez, Gabriel, Oberst, Andrew, Ofengeim, Dimitry, Opferman, Joseph T., Oren, Moshe, Pagano, Michele, Panaretakis, Theocharis, Pasparakis, Manolis, Penninger, Josef M., Pentimalli, Francesca, Pereira, David M., Pervaiz, Shazib, Peter, Marcus E., Pinton, Paolo, Porta, Giovanni, Prehn, Jochen H. M., Puthalakath, Hamsa, Rabinovich, Gabriel A., Rajalingam, Krishnaraj, Ravinchandran, Kodi S., Rehm, Markus, Ricci, Jean-Ehrland, Rizzuto, Rosario, Robinson, Nirmal, Rodrigues, Cecilia M. P., Rotblat, Barak, Rothlin, Carla V., Rubinsztein, David C., Rudel, Thomas, Rufini, Alessandro, Ryan, Kevin M., Sarosiek, Kristopher A., Sawa, Akira, Sayan, Emre, Schroder, Kate, Scorrano, Luca, Sesti, Federico, Shao, Feng, Shi, Yufang, Sica, Giuseppe, Silke, John, Simon, Hans-Uwe, Sistigu, Antonella, Stephanou, Anastasis, Stockwell, Brent R., Strappazzon, Flavie, Strasser, Andreas, Sun, Liming, Sun, Erwei, Sun, Qiang, Szabadkai, G, Tait, Stephen W. G., Tang, Daolin, Tavernarakis, Nektarios, Troy, Carol M., Turk, Boris, Urbano, Nicoletta, Vandenabeele, Peter, Vanden Berghe, Tom, Vander Heiden, Matthew G., Vanderluit, Jacqueline L., Verkhratsky, A., Villunger, Andreas, Von Karstedt, Silvia, Voss, Anne K., Vousden, Karen H., Vucic, Domagoj, Vuri, Daniela, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ruoning, Wang, Ying, Weber, Achim, Wood, Will, Yamazaki, Takahiro, Yang, Zahra, Zakeri, Zahra, Zawacka-Pankau, Joanna E., Zhang, Lin, Zhang, Haibin, Zhivotovsky, Boris, Zhou, Wenzhao, Piacentini, Mauro, Kroemer, Guido, Galluzzi, Lorenzo, Associazione Italiana per la Ricerca sul Cancro, Italian Institute for Genomic Medicine, Compagnia di San Paolo, Vitale, Ilio [0000-0002-5918-1841], Pietrocola, Federico [0000-0002-2930-234X], Guilbaud, Emma [0000-0001-5261-1944], Aaronson, Stuart A. 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[0000-0002-5444-6628], Bove, Pierluigi [0000-0002-4788-2982], Boya, Patricia [0000-0003-3045-951X], Broz, Petr [0000-0002-2334-7790], Damgaard, Rune Busk [0000-0002-1709-6534], Calin, George A. [0000-0002-7427-0578], Campanella, Michelangelo [0000-0002-6948-4184], Candi, Eleonora [0000-0001-8332-4825], Carbone, Michele [0000-0001-8928-8474], Carmona-Gutierrez, Didac [0000-0001-7548-7771], Cecconi, Francesco [0000-0002-5614-4359], Chen, Guo‑Qiang [0000-0002-7226-1782], Cheng, Emily H. [0000-0002-3595-2648], Chipuk, Jerry E. [0000-0002-1337-842X], Cidlowski, John A. [0000-0003-1420-0516], Ciechanover, Aaron [0000-0001-9184-8944], Ciliberto, Gennaro [0000-0003-2851-8605], Conrad, Marcus [0000-0003-1140-5612], Czabotar, Peter E. [0000-0002-2594-496X], D’Angiolella, Vincenzo [0000-0001-8365-9094], Daugaard, Mads [0000-0001-8383-055X], Dawson, Valina L. [0000-0002-2915-3970], De Maria, Ruggero [0000-0003-2255-0583], Debatin, Klaus-Michael [0000-0002-8397-1886], Deberardinis, Ralph J. 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G., Tang, Daolin, Tavernarakis, Nektarios, Troy, Carol M., Turk, Boris, Urbano, Nicoletta, Vandenabeele, Peter, Vanden Berghe, Tom, Vander Heiden, Matthew G., Vanderluit, Jacqueline L., Verkhratsky, A., Villunger, Andreas, Von Karstedt, Silvia, Voss, Anne K., Vousden, Karen H., Vucic, Domagoj, Vuri, Daniela, Wagner, Erwin F., Walczak, Henning, Wallach, David, Wang, Ruoning, Wang, Ying, Weber, Achim, Wood, Will, Yamazaki, Takahiro, Yang, Zahra, Zakeri, Zahra, Zawacka-Pankau, Joanna E., Zhang, Lin, Zhang, Haibin, Zhivotovsky, Boris, Zhou, Wenzhao, Piacentini, Mauro, Kroemer, Guido, and Galluzzi, Lorenzo

Abstract

Apoptosis is a form of regulated cell death (RCD) that involves proteases of the caspase family. Pharmacological and genetic strategies that experimentally inhibit or delay apoptosis in mammalian systems have elucidated the key contribution of this process not only to (post-)embryonic development and adult tissue homeostasis, but also to the etiology of multiple human disorders. Consistent with this notion, while defects in the molecular machinery for apoptotic cell death impair organismal development and promote oncogenesis, the unwarranted activation of apoptosis promotes cell loss and tissue damage in the context of various neurological, cardiovascular, renal, hepatic, infectious, neoplastic and inflammatory conditions. Here, the Nomenclature Committee on Cell Death (NCCD) gathered to critically summarize an abundant pre-clinical literature mechanistically linking the core apoptotic apparatus to organismal homeostasis in the context of disease.

Published
2023

50. Ferroptosis as a target for protection against cardiomyopathy

Author

Fang, Xuexian, Wang, Hao, Han, Dan, Xie, Enjun, Yang, Xiang, Wei, Jiayu, Gu, Shanshan, Gao, Feng, Zhu, Nali, Yin, Xiangju, Cheng, Qi, Zhang, Pan, Dai, Wei, Chen, Jinghai, Yang, Fuquan, Yang, Huang-Tian, Linkermann, Andreas, Gu, Wei, Min, Junxia, and Wang, Fudi

Published
2019

Catalog

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