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

Abstract

In conclusion, miR-125b is critical for induction of cardiac fibrosis and acts as a potent repressor of multiple anti-fibrotic mechanisms. Inhibition of miR-125b may represent a novel therapeutic approach for the treatment of human cardiac fibrosis and other fibrotic diseases.