Abstract:BackgroundThe identification of coronary artery disease-induced sudden cardiac death (CAD-SCD) has always been a medical challenge. MicroRNAs (miRNAs) played vital roles in pathogenesis processes and served as potential biomarkers for cardiovascular and many other diseases. The aim of this study was to investigate the diagnostic value of the specific miRNAs for CAD-SCD.MethodsA total of 30 autopsy-verified CAD-SCD victims were selected, including 18 individuals who experienced more than once asymptomatic myoca… Show more
“…miR-214-3p exerts an inhibitory effect on cardiac fibrosis through downregulation of NLRC5 gene expression and inhibition of the TGF-β1/Smad3 signaling pathway (30). The miR-126-5p can serve as a highly sensitive biomarker for the identification of sudden cardiac death resulting from coronary artery disease (31). The overexpression of miR-126-3p suppresses TGF-β-induced endothelial-tomesenchymal transition (EndMT) and attenuates fibroblastogenesis, thereby ameliorating fibrosis (32).…”
Section: Current Status Of Treatment For Cardiac Fibrosismentioning
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.
“…miR-214-3p exerts an inhibitory effect on cardiac fibrosis through downregulation of NLRC5 gene expression and inhibition of the TGF-β1/Smad3 signaling pathway (30). The miR-126-5p can serve as a highly sensitive biomarker for the identification of sudden cardiac death resulting from coronary artery disease (31). The overexpression of miR-126-3p suppresses TGF-β-induced endothelial-tomesenchymal transition (EndMT) and attenuates fibroblastogenesis, thereby ameliorating fibrosis (32).…”
Section: Current Status Of Treatment For Cardiac Fibrosismentioning
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.
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