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2,905 results on '"Huang, Xu"'

6. AI for organic and polymer synthesis

Author

Hong, Xin, Yang, Qi, Liao, Kuangbiao, Pei, Jianfeng, Chen, Mao, Mo, Fanyang, Lu, Hua, Zhang, Wen-Bin, Zhou, Haisen, Chen, Jiaxiao, Su, Lebin, Zhang, Shuo-Qing, Liu, Siyuan, Huang, Xu, Sun, Yi-Zhou, Wang, Yuxiang, Zhang, Zexi, Yu, Zhunzhun, Luo, Sanzhong, Fu, Xue-Feng, and You, Shu-Li

Published
2024
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23. Cirbp suppression compromises DHODH-mediated ferroptosis defense and attenuates hypothermic cardioprotection in an aged donor transplantation model

Author

Zhu, Yifan, Jiang, Chenyu, He, Jian, He, Chen, Zhou, Xingliang, Huang, Xu, Shen, Yi, Wu, Liwei, Li, Yongnan, Feng, Bei, Yan, Yi, Li, Jun, Zhang, Hao, and Liu, Yiwei

Subjects
Hypothermia, Induced -- Usage, Binding proteins -- Physiological aspects -- Health aspects, Organ donors -- Physiological aspects -- Health aspects, Age -- Physiological aspects -- Health aspects, Preservation of organs, tissues, etc. -- Methods, Heart -- Transplantation, Health care industry
Abstract

Hypothermia is commonly used to protect donor hearts during transplantation. However, patients transplanted with aged donor hearts still have severe myocardial injury and decreased survival rates, but the underlying mechanism remains unknown. Because aged hearts are not considered suitable for donation, the number of patients awaiting heart transplants is increasing. In this study, we examined whether hypothermic cardioprotection was attenuated in aged donor hearts during transplantation and evaluated potential therapeutic targets. Using a rat heart transplantation model, we found that hypothermic cardioprotection was impaired in aged donor hearts but preserved in young donor hearts. RNA-Seq showed that cold-inducible RNA-binding protein (Cirbp) expression was decreased in aged donor hearts, and these hearts showed severe ferroptosis after transplantation. The young donor hearts from Cirbp-KO rats exhibited attenuated hypothermic cardioprotection, but Cirbp overexpression in aged donor hearts ameliorated hypothermic cardioprotection. Cardiac proteomes revealed that dihydroorotate dehydrogenase (DHODH) expression was significantly decreased in Cirbp-KO donor hearts during transplantation. Consequently, DHODH-mediated ubiquinone reduction was compromised, thereby exacerbating cardiac lipid peroxidation and triggering ferroptosis after transplantation. A cardioplegic solution supplemented with CIRBP agonists improved hypothermic cardioprotection in aged donor hearts, indicating that this method has the potential to broaden the indications for using aged donor hearts in transplantation., Introduction Currently, advanced heart failure places a constant and heavy burden on clinical and public health systems (1). Treatment options for heart failure include medication, ventricular assistive devices, and heart [...]

Published
2024
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30. RED-SEA Project: Towards a new-generation European interconnect

Author

Gomez, Maria Engracia, Sahuquillo, Julio, Biagioni, Andrea, Chrysos, Nikos, Berton, Damien, Frezza, Ottorino, Lo Cicero, Francesca, Lonardo, Alessandro, Martinelli, Michele, Paolucci, Pier Stanislao, Pastorelli, Elena, Simula, Francesco, Turisini, Matteo, Vicini, Piero, Ammendola, Roberto, Chiarini, Carlotta, De Luca, Chiara, Capuani, Fabrizio, Castelló, Adrián, Duro, Jose, Stabile, Eugenio, Quintana, Enrique, Bernier-Bruna, Pascale, Chen, Claire, Lagadec, Pierre-Axel, Pichon, Gregoire, Walter, Etienne, Katevenis, Manolis, Bartzis, Sokratis, Mousouros, Orestis, Xirouchakis, Pantelis, Mageiropoulos, Vangelis, Gianioudis, Michalis, Loukas, Harisis, Ioannou, Aggelos, Kallimanis, Nikos, de la Rosa, Miguel Sanchez, Gomez-Lopez, Gabriel, Alfaro-Cortés, Francisco, Sahuquillo, Jesus Escudero, Garcia, Pedro Javier, Quiles, Francisco J., Sanchez, Jose L., De Gassowski, Gaetan, Hautreaux, Matthieu, Mathieu, Stephane, Moreau, Gilles, Perache, Marc, Taboada, Hugo, Hoefler, Torsten, Schneider, Timo, Barnaba, Matteo, Brandino, Giuseppe Piero, De Giorgi, Francesco, Poggi, Matteo, Mavroidis, Iakovos, Papaefstathiou, Yannis, Tampouratzis, Nikolaos, Kalisch, Benjamin, Krackhardt, Ulrich, Nuessle, Mondrian, Frings, Wolfang, Gottwald, Dominik, Guimaraes, Felime, Holicki, Max, Marx, Volker, Muller, Yannik, Clauss, Carsten, Falter, Hugo, Huang, Xu, Barillao, Jennifer Lopez, Moschny, Thomas, and Pickartz, Simon

Published
2024
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49. 4,8-Dicarboxyl-8,9-iridoid-1-glycoside inhibits apoptosis in human osteoarthritis chondrocytes via enhanced c-MYC-mediated cholesterol metabolism in vitro

Author

WeiBing Wang, HaiMin Mai, Huang Xu, BaoSheng Jing, CuiYu Yu, XiaoTing Li, DanGui Chen, Yuan Huang, MeiMang Shao, and Tao Pan

Subjects
Osteoarthritis, Borojoa, Cholesterol metabolism, Apoptosis, Autophagy, Diseases of the musculoskeletal system, RC925-935
Abstract

Abstract Background Osteoarthritis (OA) is a degenerative disease related to cholesterol metabolism disorders. However, current therapies for OA are insufficient and no convincing disease-modifying OA drugs exist. Therefore, we aimed to elucidate the mechanism by which borojoa iridoid glycoside (BIG) inhibits chondrocyte apoptosis in OA. Methods Borojoa pulp was heated to 70 °C, and the main active substance in borojoa, BIG, was extracted by fractionation at an ultraviolet 254-nm absorption peak. Chondrocytes were identified by immunohistochemistry and visualized by immunofluorescence confocal microscopy. The proliferation of chondrocytes cultured with BIG was determined by MTS assay. The apoptosis of chondrocytes cultured with BIG was tested by Annexin V-FITC/PI, and the cytokine, protein, and cholesterol levels in chondrocytes were detected by ELISA, RT‒qPCR, Western blot, and biochemistry analyses. Protein‒protein interactions were verified by a coimmunoprecipitation (Co-IP) assay. Results BIG promoted chondrocyte proliferation and reduced apoptosis in vitro. BIG induced an alteration of the total RNA profiles in chondrocytes, and bioinformatic analysis showed that BIG inhibited chondrocyte apoptosis by promoting c-MYC expression; KEGG analysis confirmed that BIG-inhibited apoptosis was enriched in the cell cycle pathway. Flow cell cycle experiments confirmed that BIG promoted chondrocyte proliferation by significantly increasing the S phase cell number. The c-MYC inhibitor 10058-F4 stimulated the increased expression of IL-1β, IL-6, TNF-α, and AGEs and suppressed the cholesterol metabolism, which promoted chondrocyte apoptosis and autophagy. Co-IP analysis showed that BIG promoted the interaction of c-MYC and CH25H, Bcl-2, which suggests that BIG could inhibit chondrocyte apoptosis in part by enhancing c-MYC-mediated cholesterol metabolism. Conclusions This study confirmed that BIG promotes chondrocyte proliferation and inhibits apoptosis and autophagy, and BIG improving OA is associated with cholesterol metabolism. The results identify a potential mechanism by which BIG enhances c-MYC-mediated CH25H regulation of cholesterol metabolism in vitro and suggest that BIG might be a promising new drug against OA.

Published
2023
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