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Cardiovascular Research Advance Access first published online on August 4, 2009
This version [Corrected Proof] published online on August 20, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp268
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

Matrix metalloproteinase-2 and myocardial oxidative stress injury: beyond the matrix

Arulmozhi D. Kandasamy, Ava K. Chow, Mohammad A.M. Ali and Richard Schulz*

Department of Pediatrics and Pharmacology, Cardiovascular Research Centre, 4-62 Heritage Medical Research Centre, University of Alberta, Edmonton, AB, Canada T6G 2S2

* Corresponding author. Tel: +1 780 492 6581, Fax: +1 780 492 9753, Email: richard.schulz{at}ualberta.ca

Matrix metalloproteinase (MMP)-2 belongs to a family of zinc-dependent proteases which are best known for their ability to proteolyse extracellular matrix proteins throughout the body, including the cardiovascular system. Increased MMP-2 activity has been demonstrated in myocardial ischaemia and reperfusion injury and the progression to congestive heart failure, with most evidence to date for its role in cardiac remodelling. Recent evidence, however, shows that MMP-2 also co-localizes with and proteolyses specific protein targets within the cardiomyocyte to cause acute, reversible contractile dysfunction, challenging the conventional wisdom on the ‘extracellular matrix only’ actions of this enzyme. In this review, we discuss the recent upsurge in MMP-2 research with regards to its activation by non-proteolytic pathways in the setting of enhanced oxidative stress in the heart. We will focus on the consequences of intracellular actions of MMP-2 within the cardiomyocyte and its regulation at several levels including its expression, post-translational modifications, and regulation by endogenous tissue inhibitors of metalloproteinases, caveolin, and small molecule MMP inhibitors. MMP-2 is emerging as an important signalling protease implicated in the proteolytic regulation of various intracellular proteins in myocardial oxidative stress injury.

KEYWORDS Matrix metalloproteinases; MMP-2; Oxidative stress; Ischaemia–reperfusion injury; Contractile apparatus

Time for primary review: 29 days


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