Key result
miR-486 targeting SRSF3/p21 mediates the senescence of cardiac myofibroblasts to improve fibrotic activity, limiting scar size and post-myocardial infarction remodelling.
Why the study?
Safe and curative therapies for post-MI cardiac fibrosis and pathological remodelling are lacking, and how miR-486 functions in post-MI regeneration remains unclear.
Answers are grounded in this paper and cite their sources.
miR-486 targeted silencing represents a potential novel therapeutic approach to reduce cardiac fibrosis and adverse remodeling after myocardial infarction.
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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Chen et al. (2022) studied Myocardial infarction. miR-486 was evaluated on Fibrotic activity, scar size, and post-MI remodelling. miR-486 targeting SRSF3/p21 mediates the senescence of cardiac myofibroblasts to improve fibrotic activity, limiting scar size and post-myocardial infarction remodelling.
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