Open AccessPioglitazone Alleviates Cardiac Fibrosis and Inhibits Endothelial to Mesenchymal Transition Induced by Pressure Overload
Author(s) -
Wenying Wei,
Ning Zhang,
Lingli Li,
ZhenGuo Ma,
Man Xu,
Yuan Yao,
Wei Deng,
QiZhu Tang
Publication year - 2017
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000486220
Subject(s) - pressure overload , cardiac fibrosis , smad , fibrosis , pioglitazone , muscle hypertrophy , medicine , extracellular matrix , transforming growth factor , endocrinology , chemistry , pharmacology , cardiac hypertrophy , microbiology and biotechnology , biology , diabetes mellitus , type 2 diabetes
Cardiac fibrosis, characterized by an unbalanced production and degradation of extracellular matrix components, is a common pathophysiology of multiple cardiovascular diseases. Recent studies suggested that endothelial to mesenchymal transition (EndMT) could be a source of activated fibroblasts and contribute to cardiac fibrosis. Here, the role of pioglitazone (PIO) in cardiac fibrosis and EndMT was elaborated.