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Ascending Aortic Constriction in Rats for Creation of Pressure Overload Cardiac Hypertrophy Model
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Atorvastatin attenuates cardiac hypertrophy through AMPK/miR-143-3p/Bcl2 axis

Jingang Sun1, Cuicui Zhang1, Zhigang Zhang1

  • 1Linyi Central Hospital, Yishui Linyi, China.

Archives of Physiology and Biochemistry
|July 30, 2019
PubMed

Insights

Atorvastatin protects the heart by inhibiting miR-143-3p, reducing cardiomyocyte apoptosis and cardiac hypertrophy. This mechanism involves activating the AMPK pathway and upregulating Bcl2 expression, thereby preventing heart failure.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Pharmacology

Background:

  • Atorvastatin is a lipid-lowering drug with reported cardioprotective effects.
  • The precise molecular mechanisms underlying atorvastatin's ability to attenuate cardiac hypertrophy and prevent heart failure remain largely unknown.

Purpose of the Study:

  • To elucidate the mechanism by which atorvastatin mitigates cardiac hypertrophy and inhibits cardiac failure.
  • To investigate the role of microRNA-143-3p (miR-143-3p) and Bcl2 in atorvastatin's cardioprotective effects.

Main Methods:

  • Cardiac hypertrophy was induced in rats via transverse aortic constriction (TAC) and in cardiomyocytes using angiotensin II (Ang II).
  • The expression of miR-143-3p and Bcl2 was analyzed, and the involvement of the AMP-activated protein kinase (AMPK) pathway was assessed.
  • Atorvastatin's effects on cardiac structure, apoptosis, and molecular markers were evaluated.

Main Results:

  • Atorvastatin significantly reduced TAC-induced heart weight increase and cardiomyocyte apoptosis.
  • Atorvastatin inhibited the up-regulation of miR-143-3p by activating the AMPK pathway.
  • Bcl2 was identified as a direct target of miR-143-3p, and its expression was inversely correlated with miR-143-3p levels.

Conclusions:

  • miR-143-3p exacerbates cardiac hypertrophy and apoptosis by suppressing Bcl2 expression.
  • Atorvastatin attenuates cardiac hypertrophy and prevents heart failure by inhibiting miR-143-3p via AMPK activation, leading to restored Bcl2 expression.

Keywords:
AMPK/miR-143-3p/BCL2 axisAtorvastatincardiac hypertrophy

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