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ELABELA-APJ axis protects from pressure overload heart failure and angiotensin II-induced cardiac damage

Teruki Sato1,2, Chitose Sato1, Ayumi Kadowaki1

  • 1Department of Biochemistry and Metabolic Science, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.

Cardiovascular Research
|April 4, 2017
PubMed

Insights

Elabela (ELA) peptide protects the heart from failure by suppressing angiotensin-converting enzyme (ACE) and angiotensin II signaling via the APJ receptor. This finding reveals a novel therapeutic target for cardiovascular disease.

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Endocrinology

Background:

  • Elabela (ELA) is a novel peptide ligand for the APJ receptor (APJ/Aplnr).
  • ELA is vital for early cardiac development and stem cell maintenance.
  • Apelin, another APJ ligand, impacts heart function and the renin-angiotensin system.

Purpose of the Study:

  • To investigate the cardiovascular effects of ELA.
  • To elucidate the mechanism of ELA's action in the heart.

Main Methods:

  • Infusion of ELA peptide in mice subjected to pressure overload.
  • Analysis of cardiac gene expression and fibrosis.
  • Studies in APJ knockout mice.
  • Investigation of angiotensin-converting enzyme (ACE) and ACE2 expression.
  • Assessment of FoxM1 transcription factor activity.
  • Evaluation of ELA's effect on angiotensin II-induced hypertension.

Main Results:

  • ELA significantly reduced cardiac hypertrophy, fibrosis, and contractility impairment in mice.
  • ELA decreased the expression of heart failure and fibrosis-associated genes.
  • Cardioprotective effects of ELA were dependent on APJ receptor signaling.
  • ELA downregulated ACE expression, distinct from Apelin's effects on ACE and ACE2.
  • ELA suppressed FoxM1 transcription factor activity, unlike Apelin.

Conclusions:

  • The ELA-APJ axis confers protection against pressure overload-induced heart failure.
  • ELA likely acts by suppressing ACE expression and angiotensin II signaling.
  • Differential effects of ELA and Apelin suggest ligand-specific APJ activation mechanisms.
Abstract

Keywords:
ACEACE2APJAngiotensinApelinElabela

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