MiR-125b Is Critical for Fibroblast-to-Myofibroblast Transition and Cardiac Fibrosis.

ABSTRACT:

Background

Cardiac fibrosis is the pathological consequence of stress-induced fibroblast proliferation and fibroblast-to-myofibroblast transition. MicroRNAs have been shown to play a central role in the pathogenesis of cardiac fibrosis. We identified a novel miRNA-driven mechanism that promotes cardiac fibrosis via regulation of multiple fibrogenic pathways.

Methods and results

Using a combination of in vitro and in vivo studies, we identified that miR-125b is a novel regulator of cardiac fibrosis, proliferation, and activation of cardiac fibroblasts. We demonstrate that miR-125b is induced in both fibrotic human heart and murine models of cardiac fibrosis. In addition, our results indicate that miR-125b is necessary and sufficient for the induction of fibroblast-to-myofibro

SUBMITTER: Nagpal V 

PROVIDER: S-EPMC5446084 | biostudies-literature | 2016 Jan

REPOSITORIES: biostudies-literature