miR-135a Mediates Mitochondrial Oxidative Respiratory Function through SIRT1 to Regulate Atrial Fibrosis.

Introduction: This study aimed to explore the function of miR-135a in the progress of atrial fibrosis and the mechanism of miR-135a/SIRT1 (sirtuin 1) in human cardiac fibroblasts and mouse cardiac fibroblasts (MCFs) mediating the regulation of atrial fibrosis by mitochondrial oxidative respiration function.

Methods: Using Ang II (angiotensin II) to induce fibrosis in HCFs (human corneal fibroblasts) and MCF (Michigan Cancer Foundation, MCF) cells in vitro, the miRNA-seq results of previous studies were validated. Proliferative and invasive ability of HCFs and MCFs was detected by Cell Counting Kit-8 assay (CCK-8) and scratch experiment after overexpressing miR-135a in HCFs and MCF cells.