Atorvastatin attenuates cardiac hypertrophy through AMPK/miR-143-3p/Bcl2 axis

被引:7
|
作者
Sun, Jingang [1 ]
Zhang, Cuicui [1 ]
Zhang, Zhigang [1 ]
机构
[1] Linyi Cent Hosp, 17 Jiangkang Rd, Yishui Linyi 276400, Shandong, Peoples R China
关键词
Atorvastatin; cardiac hypertrophy; AMPK; miR-143-3p; BCL2; axis; HEART-FAILURE; APOPTOSIS; INHIBITORS; EXPRESSION; MECHANISM; MODEL;
D O I
10.1080/13813455.2019.1643377
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Atorvastatin is employed as a lipid lowering agent and its heart protective effect has been recently reported as well. However, the mechanism of atorvastatin in attenuating cardiac hypertrophy and inhibiting cardiac failure is unclear. In our study, cardiac hypertrophy was induced in rats using transverse aortic constriction (TAC) method and in cardiomyocytes using angiotensin II (Ang II). Atorvastatin significantly suppressed TAC-induced heart weight increase and cardiomyocytes apoptosis in rats. At a molecular level, we found that miR-143-3p was significantly up-regulated, and the up-regulation could be inhibited by atorvastatin via activating AMPK pathway. Furthermore, it was validated that Bcl2 was one of the target genes of miR-143-3p. Taken together, the data indicated that miR-143-3p aggravated cardiac hypertrophy by inducing cardiomyocytes apoptosis through inhibiting Bcl2 expression. This study demonstrated the effects of atorvastatin in attenuating cardiac hypertrophy and inhibiting cardiac failure, which is depending on Bcl2 expression via miR-143-3p inhibition by AMPK activation.
引用
收藏
页码:390 / 396
页数:7
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