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10.1080/15384101.2019.1580494

http://scihub22266oqcxt.onion/10.1080/15384101.2019.1580494
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C6464590!6464590!30810438
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suck abstract from ncbi


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pmid30810438      Cell+Cycle 2019 ; 18 (5): 621-37
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  • Overexpression of microRNA-202-3p protects against myocardial ischemia-reperfusion injury through activation of TGF-?1/Smads signaling pathway by targeting TRPM6 #MMPMID30810438
  • Wu HY; Wu JL; Ni ZL
  • Cell Cycle 2019[]; 18 (5): 621-37 PMID30810438show ga
  • MicroRNAs (miRNAs) have been found to act as key regulators in the pathogenesis of myocardial ischemic-reperfusion (I/R) injury. In this study, we explore the role and mechanism of microRNA-202-3p (miR-202-3p) in regulating cardiomyocyte apoptosis, in respective of the TGF-?1/Smads signaling pathway by targeting the transient receptor potential cation channel, subfamily M, member 6 (TRPM6). The targeting relationship between miR-202-3p and TRPM6 was verified by a dual-luciferase reporter gene assay. Sprague-Dawley rat models of myocardial I/R injury were initially established and treated with different mimics, inhibitors and siRNAs to test the effects of miR-202-3p and TRPM6 on myocardial I/R injury. The levels of inflammatory factors; IL-1?, IL-6, TNF-? as well as the degree of myocardial fibrosis and cardiomyocyte apoptosis were determined in rats transfected with different plasmids. TRPM6 was found to be the target of miR-202-3p. Up-regulated miR-202-3p or knockdown of TRPM-6 alleviated oxidative stress and inflammatory response, reduced ventricular mass, altered cardiac hemodynamics, suppressed myocardial infarction, attenuated cell apoptosis, and inhibited myocardial fibrosis. MiR-202-3p overexpression activates the TGF-?1/Smads signaling pathway by negatively regulating TRPM6 expression. Taken together, these findings suggest that miR-202-3p offers protection against ventricular remodeling after myocardial I/R injury via activation of the TGF-?1/Smads signaling pathway.
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