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Your search keyword '"Suárez, Yajaira"' showing total 9 results
Start Over Author "Suárez, Yajaira" Publisher american society for clinical investigation
9 results on '"Suárez, Yajaira"'

1. Hepatocyte-specific suppression of ANGPTL4 improves obesity-associated diabetes and mitigates atherosclerosis in mice

Author

Singh, Abhishek K., primary, Chaube, Balkrishna, additional, Zhang, Xinbo, additional, Sun, Jonathan, additional, Citrin, Kathryn M., additional, Canfrán-Duque, Alberto, additional, Aryal, Binod, additional, Rotllan, Noemi, additional, Varela, Luis, additional, Lee, Richard G., additional, Horvath, Tamas L., additional, Price, Nathan L., additional, Suárez, Yajaira, additional, and Fernández-Hernando, Carlos, additional

Published
2021
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3. Genetic deficiency or pharmacological inhibition of miR-33 protects from kidney fibrosis

Author

Price, Nathan L., primary, Miguel, Verónica, additional, Ding, Wen, additional, Singh, Abhishek K., additional, Malik, Shipra, additional, Rotllan, Noemi, additional, Moshnikova, Anna, additional, Toczek, Jakub, additional, Zeiss, Caroline, additional, Sadeghi, Mehran M., additional, Arias, Noemi, additional, Baldán, Ángel, additional, Andreev, Oleg A., additional, Rodríguez-Puyol, Diego, additional, Bahal, Raman, additional, Reshetnyak, Yana K., additional, Suárez, Yajaira, additional, Fernández-Hernando, Carlos, additional, and Lamas, Santiago, additional

Published
2019
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4. Suppressing miR-21 activity in tumor-associated macrophages promotes an antitumor immune response

Author

Sahraei, Mahnaz, primary, Chaube, Balkrishna, additional, Liu, Yuting, additional, Sun, Jonathan, additional, Kaplan, Alanna, additional, Price, Nathan L., additional, Ding, Wen, additional, Oyaghire, Stanley, additional, García-Milian, Rolando, additional, Mehta, Sameet, additional, Reshetnyak, Yana K., additional, Bahal, Raman, additional, Fiorina, Paolo, additional, Glazer, Peter M., additional, Rimm, David L., additional, Fernández-Hernando, Carlos, additional, and Suárez, Yajaira, additional

Published
2019
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5. Genetic deficiency or pharmacological inhibition of miR-33 protects from kidney fibrosis.

Author

American Heart Association, Fondation Leducq, University of Connecticut, Ministerio de Economía y Competitividad (España), Instituto de Salud Carlos III, Comunidad de Madrid, Sociedad Española de Nefrología, Fundación Renal Íñigo Álvarez de Toledo, Fundación Ramón Areces, Ministerio de Educación, Cultura y Deporte (España), Price, Nathan L., Miguel, Verónica, Ding, Wen, Singh, Abhishek K., Malik,Shipra, Rotllan,Noemi, Moshnikova, Anna, Toczek, Jakub, Zeiss, Caroline, Sadeghi, Mehran M., Arias, Noemi, Baldán, Ángel, Andreev, Oleg A., Rodríguez-Puyol, Diego, Bahal, Raman, Reshetnyak, Yana K., Suárez, Yajaira, Fernández-Hernando, Carlos, Lamas Peláez, Santiago, American Heart Association, Fondation Leducq, University of Connecticut, Ministerio de Economía y Competitividad (España), Instituto de Salud Carlos III, Comunidad de Madrid, Sociedad Española de Nefrología, Fundación Renal Íñigo Álvarez de Toledo, Fundación Ramón Areces, Ministerio de Educación, Cultura y Deporte (España), Price, Nathan L., Miguel, Verónica, Ding, Wen, Singh, Abhishek K., Malik,Shipra, Rotllan,Noemi, Moshnikova, Anna, Toczek, Jakub, Zeiss, Caroline, Sadeghi, Mehran M., Arias, Noemi, Baldán, Ángel, Andreev, Oleg A., Rodríguez-Puyol, Diego, Bahal, Raman, Reshetnyak, Yana K., Suárez, Yajaira, Fernández-Hernando, Carlos, and Lamas Peláez, Santiago

Abstract

Previous work has reported the important links between cellular bioenergetics and the development of chronic kidney disease, highlighting the potential for targeting metabolic functions to regulate disease progression. More recently, it has been shown that alterations in fatty acid oxidation (FAO) can have an important impact on the progression of kidney disease. In this work, we demonstrate that loss of miR-33, an important regulator of lipid metabolism, can partially prevent the repression of FAO in fibrotic kidneys and reduce lipid accumulation. These changes were associated with a dramatic reduction in the extent of fibrosis induced in 2 mouse models of kidney disease. These effects were not related to changes in circulating leukocytes because bone marrow transplants from miR-33–deficient animals did not have a similar impact on disease progression. Most important, targeted delivery of miR-33 peptide nucleic acid inhibitors to the kidney and other acidic microenvironments was accomplished using pH low insertion peptides as a carrier. This was effective at both increasing the expression of factors involved in FAO and reducing the development of fibrosis. Together, these findings suggest that miR-33 may be an attractive therapeutic target for the treatment of chronic kidney disease

Published
2019

6. Inhibition of profibrotic microRNA-21 affects platelets and their releasate

Author

Barwari, Temo, primary, Eminaga, Seda, additional, Mayr, Ursula, additional, Lu, Ruifang, additional, Armstrong, Paul C., additional, Chan, Melissa V., additional, Sahraei, Mahnaz, additional, Fernández-Fuertes, Marta, additional, Moreau, Thomas, additional, Barallobre-Barreiro, Javier, additional, Lynch, Marc, additional, Yin, Xiaoke, additional, Schulte, Christian, additional, Baig, Ferheen, additional, Pechlaner, Raimund, additional, Langley, Sarah R., additional, Zampetaki, Anna, additional, Santer, Peter, additional, Weger, Martin, additional, Plasenzotti, Roberto, additional, Schosserer, Markus, additional, Grillari, Johannes, additional, Kiechl, Stefan, additional, Willeit, Johann, additional, Shah, Ajay M., additional, Ghevaert, Cedric, additional, Warner, Timothy D., additional, Fernández-Hernando, Carlos, additional, Suárez, Yajaira, additional, and Mayr, Manuel, additional

Published
2018
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7. Absence of ANGPTL4 in adipose tissue improves glucose tolerance and attenuates atherogenesis

Author

Aryal, Binod, primary, Singh, Abhishek K., additional, Zhang, Xinbo, additional, Varela, Luis, additional, Rotllan, Noemi, additional, Goedeke, Leigh, additional, Chaube, Balkrishna, additional, Camporez, Joao-Paulo, additional, Vatner, Daniel F., additional, Horvath, Tamas L., additional, Shulman, Gerald I., additional, Suárez, Yajaira, additional, and Fernández-Hernando, Carlos, additional

Published
2018
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8. Inhibition of profibrotic microRNA-21 affects platelets and their releasate

Author

Barwari, Temo, Eminaga, Seda, Mayr, Ursula, Lu, Ruifang, Armstrong, Paul C, Chan, Melissa V, Sahraei, Mahnaz, Fernández-Fuertes, Marta, Moreau, Thomas, Barallobre-Barreiro, Javier, Lynch, Marc, Yin, Xiaoke, Schulte, Christian, Baig, Ferheen, Pechlaner, Raimund, Langley, Sarah R, Zampetaki, Anna, Santer, Peter, Weger, Martin, Plasenzotti, Roberto, Schosserer, Markus, Grillari, Johannes, Kiechl, Stefan, Willeit, Johann, Shah, Ajay M, Ghevaert, Cedric, Warner, Timothy D, Fernández-Hernando, Carlos, Suárez, Yajaira, and Mayr, Manuel

Subjects
Platelets, Blood Platelets, Male, Proteomics, RNA, Untranslated, Noncoding RNAs, Cardiology, Transforming Growth Factor beta1, Mice, Animals, Humans, Prospective Studies, Aged, Aged, 80 and over, Clinical Trials as Topic, Myocardium, Cell Biology, Fibroblasts, Middle Aged, Fibrosis, 3. Good health, Extracellular Matrix, Mice, Inbred C57BL, MicroRNAs, Female, Wiskott-Aldrich Syndrome Protein
Abstract

Fibrosis is a major contributor to organ disease for which no specific therapy is available. MicroRNA-21 (miR-21) has been implicated in the fibrogenetic response, and inhibitors of miR-21 are currently undergoing clinical trials. Here, we explore how miR-21 inhibition may attenuate fibrosis using a proteomics approach. Transfection of miR-21 mimic or inhibitor in murine cardiac fibroblasts revealed limited effects on extracellular matrix (ECM) protein secretion. Similarly, miR-21-null mouse hearts showed an unaltered ECM composition. Thus, we searched for additional explanations as to how miR-21 might regulate fibrosis. In plasma samples from the community-based Bruneck Study, we found a marked correlation of miR-21 levels with several platelet-derived profibrotic factors, including TGF-β1. Pharmacological miR-21 inhibition with an antagomiR reduced the platelet release of TGF-β1 in mice. Mechanistically, Wiskott-Aldrich syndrome protein, a negative regulator of platelet TGF-β1 secretion, was identified as a direct target of miR-21. miR-21-null mice had lower platelet and leukocyte counts compared with littermate controls but higher megakaryocyte numbers in the bone marrow. Thus, to our knowledge this study reports a previously unrecognized effect of miR-21 inhibition on platelets. The effect of antagomiR-21 treatment on platelet TGF-β1 release, in particular, may contribute to the antifibrotic effects of miR-21 inhibitors.

9. miR-33 deletion in hepatocytes attenuates MASLD-MASH-HCC progression.

Author

Fernández-Tussy P, Cardelo MP, Zhang H, Sun J, Price NL, Boutagy NE, Goedeke L, Cadena-Sandoval M, Xirouchaki CE, Brown W, Yang X, Pastor-Rojo O, Haeusler RA, Bennett AM, Tiganis T, Suárez Y, and Fernández-Hernando C

Subjects
Animals, Mice, Humans, Lipid Metabolism genetics, Male, Fatty Liver genetics, Fatty Liver metabolism, Fatty Liver pathology, Mice, Knockout, Disease Models, Animal, Liver metabolism, Liver pathology, MicroRNAs genetics, MicroRNAs metabolism, Hepatocytes metabolism, Hepatocytes pathology, Carcinoma, Hepatocellular genetics, Carcinoma, Hepatocellular pathology, Carcinoma, Hepatocellular metabolism, Disease Progression, Liver Neoplasms genetics, Liver Neoplasms pathology, Liver Neoplasms metabolism
Abstract

The complexity of the mechanisms underlying metabolic dysfunction-associated steatotic liver disease (MASLD) progression remains a significant challenge for the development of effective therapeutics. miRNAs have shown great promise as regulators of biological processes and as therapeutic targets for complex diseases. Here, we study the role of hepatic miR-33, an important regulator of lipid metabolism, during the progression of MASLD and the development of hepatocellular carcinoma (HCC). We report that miR-33 was elevated in the livers of humans and mice with MASLD and that its deletion in hepatocytes (miR-33 HKO) improved multiple aspects of the disease, including steatosis and inflammation, limiting the progression to metabolic dysfunction-associated steatotic hepatitis (MASH), fibrosis, and HCC. Mechanistically, hepatic miR-33 deletion reduced lipid synthesis and promoted mitochondrial fatty acid oxidation, reducing lipid burden. Additionally, absence of miR-33 altered the expression of several known miR-33 target genes involved in metabolism and resulted in improved mitochondrial function and reduced oxidative stress. The reduction in lipid accumulation and liver injury resulted in decreased YAP/TAZ pathway activation, which may be involved in the reduced HCC progression in HKO livers. Together, these results suggest suppressing hepatic miR-33 may be an effective therapeutic approach to temper the development of MASLD, MASH, and HCC in obesity.

Published
2024
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