Mir-21 Promotes Cardiac Fibrosis After Myocardial Infarction Via Targeting Smad7 - Yuan, Jinxia; Chen, Hongtao; Ge, Dawei; Xu, Yu; Xu, Haihua; Yang, Yang; Gu, Ming; Zhou, Yuhe; Zhu, Jingdong; Ge, Ting; Chen, Qun; Gao, Yue; et al. (Cellular physiology and biochemistry, 2017)
Keywords: Animals; Antagomirs - metabolism; Cardiac fibrosis; Cell Survival - drug effects; Cells, Cultured; Disease Models, Animal; Fibroblasts; Fibroblasts - cytology; Fibroblasts - drug effects; Fibroblasts - metabolism; Fibrosis; Gene expression; Heart attacks; Heart failure; Male; Mice; Mice, Inbred C57BL; MicroRNAs - antagonists & inhibitors; MicroRNAs - genetics; MicroRNAs - metabolism; Mir-21; Mortality; Myocardial infarction; Myocardial Infarction - metabolism; Myocardial Infarction - pathology; Myocardium - cytology; Myocardium - metabolism; Original Paper; Ostomy; Rats; Rats, Sprague-Dawley; RNA Interference; Rodents; Roles; Signal Transduction - drug effects; Smad7; Smad7 Protein - antagonists & inhibitors; Smad7 Protein - genetics; Smad7 Protein - metabolism; Surgery; TGF-β1; Traditional Chinese medicine; Transforming Growth Factor beta1 - pharmacology; Up-Regulation - drug effects; United States--US; China; Myocardial infarction; Cardiac fibrosis; TGF-β1; Smad7; Mir-21