Exercise improves cardiac fibrosis by stimulating the release of endothelial progenitor cell-derived exosomes and upregulating miR-126 expression
Fu G., Wang Z., Hu S.
Narrative Review on Cardiovascular Disease, published in Front Cardiovasc Med (2024) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Narrative Review
- Journal
- Front Cardiovasc Med (2024)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 38798919
- PMCID
- PMC11119291
- DOI
- 10.3389/fcvm.2024.1323329
- Citations
- 15
Abstract (original English)
Cardiac fibrosis is an important pathological manifestation of various cardiac diseases such as hypertension, coronary heart disease, and cardiomyopathy, and it is also a key link in heart failure. Previous studies have confirmed that exercise can enhance cardiac function and improve cardiac fibrosis, but the molecular target is still unclear. In this review, we introduce the important role of miR-126 in cardiac protection, and find that it can regulate TGF-β/Smad3 signaling pathway, inhibit cardiac fibroblasts transdifferentiation, and reduce the production of collagen fibers. Recent studies have shown that exosomes secreted by cells can play a specific role through intercellular communication through the microRNAs carried by exosomes. Cardiac endothelial progenitor cell-derived exosomes (EPC-Exos) carry miR-126, and exercise training can not only enhance the release of exosomes, but also up-regulate the expression of miR-126. Therefore, through derivation and analysis, it is believed that exercise can inhibit TGF-β/Smad3 signaling pathway by up-regulating the expression of miR-126 in EPC-Exos, thereby weakening the transdifferentiation of cardiac fibroblasts into myofibroblasts. This review summarizes the specific pathways of exercise to improve cardiac fibrosis by regulating exosomes, which provides new ideas for exercise to promote cardiovascular health.
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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