Cardiac fibrosis is an integral part of many heart diseases. Characterized by an excessive deposition of the extracellular matrix (ECM) within cardiac interstitial spaces, it exacerbates the passive stiffness of the myocardium leading to progressive heart dysfunction. The condition culminates in fatal arrhythmias and heart failure (Hf). Under pathological stress and environmental stimulus, cardiac fibroblasts (CFs), a major cellular group in the heart responsible for ECM homeostasis, transition into myofibroblasts. This transition alters ECM production and degradation, thus advancing cardiac fibrosis. Given the lack of safe and effective treatment options, there is a need for novel modulatory agents and potential therapeutic targets to be identified for clinical intervention. Learn more: IgE and miR-486A-5p: Potential Therapeutic Targets for Cardiac Fibrosis
