Suppression of miR-143-3p contributes to the anti-fibrosis effect of atorvastatin on myocardial tissues via the modulation of Smad2 activity.

Atorvastatin is a commonly prescribed statin drug for the control of lipid synthesis and recent studies have shown the cardiac protection potential of atorvastatin. Cardiac fibrosis is a critical process that impairs heart function. In the current study, the anti-fibrosis potential of atorvastatin was assessed and the mechanism associated with the treatment was explored. Fibrotic symptoms were induced using transverse aortic constriction (TAC) method in vivo and using TGF-β1 in vitro. The effect of atorvastatin on the development of cardiac fibrosis was firstly measured. Moreover, the influence of miR-143-3p induction on the anti-fibrosis function of atorvastatin was determined. TAC administration induced cardiac fibrosis and heart weight increase, which was associated with the induced expressions of TGF-β1, miR-143-3p, p-Smad2, and collagens. Atorvastatin restored the levels of TGF-β1, miR-143-3p, p-Smad2, and collagens. The administration of TGF-β1 induced the expressions of miR-143-3p, p-Smad2, and collagens in cardiac fibroblasts (CFs) and the effect was inhibited by atorvastatin. However, the function of atorvastatin was blocked by miR-143-3p mimics. The current study demonstrated that the suppression of miR-143-3p contributed to the anti-fibrosis effect of atorvastatin on myocardial tissues, which subsequently inhibited Smad2-mediated production of collagens.