Title:Statins Attenuate Fibrotic Manifestations of Cardiac Tissue Damage
Volume: 14
Author(s): Armita M. Gorabi, Nasim Kiaie, Vanessa Bianconi, Matteo Pirro, Tannaz Jamialahmadi and Amirhossein Sahebkar*
Affiliation:
- Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad,Iran
Keywords:
Statins, fibrosis, hypertrophy, cardiomyopathy, pleiotropic effects, tissue damage.
Abstract: Cardiac fibrosis is a maladaptive condition secondary to cardiomyopathy caused by a
wide spectrum of stimuli, including myocardial 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 in undesirable outcomes like the disruption of excitation-contraction
coupling and ventricular hypertrophy, leading finally to 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
has 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 crosstalk
between cells in cardiac tissue as well as altering the expression and function of different
molecules involved in cardiac remodeling, including 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 in the inhibition
of fibrotic and hypertrophic remodeling in the heart, thereby potentially helping to recover proper
cardiac size, plasticity, and functioning.
