<scp>miR</scp>‐486 improves fibrotic activity in myocardial infarction by targeting <scp>SRSF3</scp>/<scp>p21‐Mediated</scp> cardiac myofibroblast senescence
Hongyi Chen, Luocheng Lv, Ruoxu Liang, Weimin Guo, Zhaofu Liao, Yilin Chen, Kuikui Zhu, Ruijin Huang, Hui Zhao, Pu Qin, Ziqiang Yuan, Zhaohua Zeng, Xin Zheng, Shanshan Feng, Xufeng Qi, Dongqing Cai
Abstract
The regulation of fibrotic activities is key to improving pathological remodelling post-myocardial infarction (MI). Currently, in the clinic, safe and curative therapies for cardiac fibrosis and improvement of the pathological fibrotic environment, scar formation and pathological remodelling post-MI are lacking. Previous studies have shown that miR-486 is involved in the regulation of fibrosis. However, it is still unclear how miR-486 functions in post-MI regeneration. Here, we first demonstrated that miR-486 targeting SRSF3/p21 mediates the senescence of cardiac myofibroblasts to improve their fibrotic activity, which benefits the regeneration of MI by limiting scar size and post-MI remodelling. miR-486-targeted silencing has high potential as a novel target to improve fibrotic activity, cardiac fibrosis and pathological remodelling.