miR‐486 improves fibrotic activity in myocardial infarction by targeting SRSF3/p21‐Mediated cardiac myofibroblast senescence

miR‐486 improves fibrotic activity in myocardial infarction by targeting SRSF3/p21‐Mediated cardiac myofibroblast senescence

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...

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Published in:Journal of cellular and molecular medicine Vol. 26; no. 20; pp. 5135 - 5149
Main Authors: Chen, Hongyi, Lv, Luocheng, Liang, Ruoxu, Guo, Weimin, Liao, Zhaofu, Chen, Yilin, Zhu, Kuikui, Huang, Ruijin, Zhao, Hui, Pu, Qin, Yuan, Ziqiang, Zeng, Zhaohua, Zheng, Xin, Feng, Shanshan, Qi, Xufeng, Cai, Dongqing
Format: Journal Article
Language:English
Published: Chichester John Wiley & Sons, Inc 01-10-2022
John Wiley and Sons Inc
Subjects:
Apoptosis
Cardiomyocytes
Cell cycle
Cyclin-dependent kinase inhibitor p21
Fibroblasts
Fibrosis
Fitness equipment
Flow cytometry
Gene expression
Heart
Heart attacks
Ischemia
MicroRNAs
miR‐486
Myocardial infarction
Original
regeneration of myocardial infarction
Senescence
senescence of cardiac myofibroblasts
SRSF3
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Summary: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.
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ISSN:1582-1838
1582-4934
DOI:10.1111/jcmm.17539