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(Pro)renin Receptor Blockade Ameliorates Cardiac Injury and Remodeling and Improves Function After

Leigh J Ellmers1, Miriam T Rademaker1, Christopher J Charles1

  • 1Department of Medicine, Christchurch Heart Institute, University of Otago, Christchurch, New Zealand.

Journal of Cardiac Failure
|September 13, 2015
PubMed
Abstract

Insights

Blocking the (pro)renin receptor [(P)RR] after myocardial infarction (MI) in mice significantly improved cardiac function and reduced infarct size. This suggests (P)RR is a promising therapeutic target for treating heart damage post-MI.

Area of Science:

  • Cardiovascular Research
  • Molecular Cardiology
  • Pharmacology

Background:

  • The (pro)renin receptor [(P)RR] plays a role in cardiovascular disease.
  • Investigating (P)RR blockade's effects post-myocardial infarction (MI) is crucial.

Purpose of the Study:

  • To evaluate the therapeutic potential of (P)RR blockade in a mouse model of MI.
  • To determine if inhibiting (P)RR can mitigate cardiac dysfunction and damage after MI.

Main Methods:

  • Myocardial infarction (MI) was induced in mice via coronary ligation.
  • Mice received either vehicle control or a (P)RR antagonist for 28 days post-MI.
  • Cardiac function, infarct size, fibrosis, and gene expression were assessed.

Main Results:

  • MI significantly reduced left ventricular ejection fraction and fractional shortening, while increasing cardiac volumes and fibrosis.
  • (P)RR antagonism post-MI improved cardiac function (LVEF, fractional shortening, stroke volume).
  • (P)RR blockade reduced infarct size, cardiac fibrosis, cardiomyocyte diameter, and expression of pro-fibrotic and hypertrophic markers.

Conclusions:

  • (P)RR blockade effectively ameliorates cardiac dysfunction and pathological remodeling following MI in mice.
  • The (pro)renin receptor represents a potential therapeutic target for managing myocardial infarction.
  • Targeting (P)RR may offer a novel strategy to improve outcomes after heart attack.
Keywords:
(Pro)renin receptorcardiac fibrosiscardiac remodellingleft ventricular functionmyocardial infarction

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