The miR-214-3p/c-Ski axis modulates endothelial-mesenchymal transition in human coronary artery endothelial cells in vitro and in mice model in vivo.

Cardiovascular disease (CVD) is a leading non-communicable disease with a high fatality rate worldwide. Hypertension, a common cardiovascular condition, is a significant risk factor for the development of heart failure because the activation of the renin-angiotensin system (RAS) is considered to be the major promoting reason behind myocardial fibrosis (MF). In this study, Angiotensin II (Ang II) stimulation-induced endothelial to mesenchymal transition (End-MT) in HCAECs, including the decrease of CD31 level, the increase of α-SMA, collagen I, slug, snail, and TGF-β1 levels, and the promotion of Smad2/3 phosphorylation.

NR4A3 induces endothelial dysfunction through up-regulation of endothelial 1 expression in adipose tissue-derived stromal cells.

Hypertension is one of the most prevalent diseases worldwide. Increased synthesis of the vasoconstrictor peptide endothelin 1 (encoded by EDN1) might be responsible for high blood pressure. The present study further confirmed the abnormal EDN1 upregulation within adipose tissue-derived stromal cells (ADSCs) derived from morbidly obese subjects.

Cox-2 promotes mesenchymal stem cells differentiation into cardiocytes by activating JNK and ERK pathway.

Coronary heart disease and various cardiomyopathys may cause myocardial damage, reducing the number of myocardial cells with complete functions. Cyclooxygenase 2 (Cox-2) has been reported participating in a variety of pathological processes, including tumor invasion and metastasis. In this study, we sought to explore the correlation of Cox-2 with MSCs proliferation, and migration.