4.3 Article

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

Journal

ARCHIVES OF PHYSIOLOGY AND BIOCHEMISTRY
Volume 127, Issue 5, Pages 390-396

Publisher

TAYLOR & FRANCIS LTD
DOI: 10.1080/13813455.2019.1643377

Keywords

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

Ask authors/readers for more resources

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.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.3
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available