Statins Attenuate Fibrotic Manifestations of Cardiac Tissue Damage

(E-pub Ahead of Print)

Author(s): Armita Mahdavi Gorabi, Nasim Kiaie, Vanessa Bianconi, Matteo Pirro, Tannaz Jamialahmadi, Amirhossein Sahebkar*

Journal Name: Current Molecular Pharmacology

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Cardiac fibrosis is a maladaptive condition secondary to cardiomyopathy caused by a wide spectrum of stimuli includingmyocardial infarction (MI), pressure overload, hyperglycemia, aging, and other factors.Despite having been supposed to be a reparative mechanism, the development of cardiac fibrosis can result inundesirable outcomes likedisruption of excitation-contraction coupling and ventricular hypertrophy leading finallyto heart failure (HF).Statins are known as potent cardioprotective agents widely used to control dyslipidemia; these drugs have exhibited protective effects against manifestations of cardiac fibrosis and hypertrophy.Cumulative evidence have suggested that statins attenuate the severity of fibrotic and hypertrophic manifestations of cardiac damage by affecting a variety of mechanisms like differentiation of myofibroblasts and cross-talk between cells in cardiac tissue as well as altering the expression and function of different molecules involved in cardiac remodelingincluding inflammatory cytokines and signaling molecules.It seems that statins can inhibit cardiac fibrosis and hypertrophy not only through their ability to inhibit hydroxymethylglutaryl-CoA reductase, but also by their pleiotropic properties.This review aims to discuss the effects of statins on molecular pathways involved inthe inhibition of fibrotic and hypertrophic remodeling in the heart, therebypotentially helping to recover proper cardiac size, plasticity, and functioning.

Keywords: statins, fibrosis, hypertrophy, cardiomyopathy, pleiotropic effects

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Article Details

Published on: 10 February, 2021
(E-pub Ahead of Print)
DOI: 10.2174/1874467214666210210123206
Price: $95

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