MiR-210 overexpression increases pressure overload-induced cardiac fibrosis.

ABSTRACT: Aortic stenosis, a common valvular heart disease, can lead to left ventricular pressure overload, triggering pro-fibrotic responses in the heart. miR-210 is a microRNA that responds to hypoxia and ischemia and plays a role in immune regulation and in cardiac remodeling upon myocardial infarction. This study investigated the effects of miR-210 on cardiac fibrosis caused by pressure overload. Using a mouse model with inducible miR-210 over-expression, we subjected mice to transverse aortic constriction (TAC) to induce pressure overload. Mice with miR-210 over-expression developed eccentric hypertrophy, heightened expression of hypertrophic markers (Nppa and Nppb) and increased cross sectional area of cardiomyocytes, impacting the free wall of the left ventricle. These findings suggest that m

SUBMITTER: Zaccagnini G 

PROVIDER: S-EPMC11874870 | biostudies-literature | 2025 Jun

REPOSITORIES: biostudies-literature