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Biochem Pharmacol. 2008 May 15;75(10):1882-92. doi: 10.1016/j.bcp.2007.12.015. Epub 2008 Jan 5.

The apelin-APJ system in heart failure: pathophysiologic relevance and therapeutic potential.

Author information

1
Centre for Cardiovascular Science, University of Edinburgh, Chancellor's Building, Edinburgh EH16 4SB, United Kingdom. alan.japp@ed.ac.uk

Abstract

Apelin is the endogenous ligand for the previously orphaned G protein-coupled receptor, APJ. This novel peptidic signalling pathway is widely represented in the heart and vasculature, and is emerging as an important regulator of cardiovascular homeostasis. In preclinical models, apelin causes nitric oxide-dependent vasodilatation, reduces ventricular preload and afterload, and increases cardiac contractility in rats with normal and failing hearts. Apelin-APJ signalling also attenuates ischemic myocardial injury and maintains cardiac performance in ageing and chronic pressure overload. Downregulation of apelin and APJ expression coincides with declining cardiac performance raising the possibility that diminished apelin-APJ activity may have pathophysiologic implications. At present, data from human studies is limited but changes in apelin and APJ expression in patients with chronic heart failure parallel those seen in preclinical models. Detailed clinical investigation is now required to establish the role of apelin in human cardiovascular physiology and pathophysiology, and to determine the therapeutic potential of augmenting apelin signalling in patients with heart failure.

PMID:
18272138
DOI:
10.1016/j.bcp.2007.12.015
[Indexed for MEDLINE]

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