4.3 Article

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

期刊

ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY
卷 127, 期 5, 页码 390-396

出版社

TAYLOR & FRANCIS LTD
DOI: 10.1080/13813455.2019.1643377

关键词

Atorvastatin; cardiac hypertrophy; AMPK; miR-143-3p; BCL2 axis

向作者/读者索取更多资源

Atorvastatin attenuates cardiac hypertrophy and inhibits cardiac failure by activating the AMPK pathway to suppress miR-143-3p, which induces cardiomyocytes apoptosis and affects Bcl2 expression.
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.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.3
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据