TGF-β1/SMAD3 Regulates Programmed Cell Death 5 That Suppresses Cardiac Fibrosis Post–Myocardial Infarction by Inhibiting HDAC3

Progressive cardiac fibrosis leads to ventricular wall stiffness, cardiac dysfunction, and eventually heart failure, but the underlying mechanism remains unexplored. PDCD5 (programmed cell death 5) ubiquitously expresses in tissues, including the heart; however, the role of PDCD5 in cardiac fibrosis...

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Veröffentlicht in:	Circulation research 2023-07, Vol.133 (3), p.237-251
Hauptverfasser:	Weng, Lin, Ye, Jingjing, Yang, Fenghe, Jia, Shi, Leng, Minghong, Jia, Bo, Xu, Chunling, Zhao, Yang, Liu, Ruxia, Xiong, Yufei, Zhou, Yiqing, Zhao, Junhui, Zheng, Ming
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Apoptosis Fibroblasts - metabolism Fibrosis Heart Mice Myocardial Infarction - metabolism Myocardium - metabolism Smad3 Protein - metabolism Transforming Growth Factor beta1 - metabolism
Online-Zugang:	Volltext
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