Abstract
High salt can induce cardiac damage. The aim of this present study was to explore the effect and the mechanism of microRNA (miR)-142-3p on the cardiac fibrosis induced by high salt. Rats received high salt diet to induce cardiac fibrosis in vivo, and neonatal rat cardiac fibroblasts (NRCF) treated with sodium chloride (NaCl) to induce fibrosis in vitro. The fibrosis and mitochondrial autophagy levels were increased the heart and NRCF treated with NaCl, which were alleviated by miR-142-3p upregulation. The fibrosis and mitochondrial autophagy levels were elevated in NRCF after treating with miR-142-3p antagomiR. Optineurin (OPTN) expression was increased in the mitochondria of NRCF induced by NaCl, which was attenuated by miR-142-3p agomiR. OPTN downregulation inhibited the increases of fibrosis and mitochondrial autophagy levels induced by NaCl in NRCF. These results miR-142-3p could alleviate high salt-induced cardiac fibrosis via downregulation of OPTN to reduce mitophagy.