Exercise and cardiac fibrosis

Abstract

Cardiac fibrosis is an important pathological process leading to heart failure, characterized by the deposition of extracellular matrix proteins in the myocardial interstitium disrupting the normal structure and function of the myocardium. In this review, we summarized the underlying mechanisms by which exercise can exert cardioprotective effects by inhibiting cardiac fibrosis. In general, this review discussed that exercise promotes the secretion of cardioprotective exerkines, inhibits systemic activation of the renin–angiotensin system axis and sympathetic overactivation, attenuates oxidative stress and inflammatory responses, and regulates metabolism and noncoding RNA. In conclusion, our review may provide a current understanding of the mechanisms by which exercise acts as an important nonpharmacological strategy to intervene in cardiac fibrosis for cardioprotection.