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Cardiovascular Research Advance Access first published online on December 2, 2008
This version [Corrected Proof] published online on December 16, 2008
Cardiovascular Research, doi:10.1093/cvr/cvn333
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org.

Myocardial repair/remodelling following infarction: roles of local factors

Yao Sun*

Division of Cardiovascular Diseases, Department of Medicine, University of Tennessee Health Science Center, 956 Court Avenue, Box 20, Memphis, TN 38163, USA

* Corresponding author. Tel: +1 901 448 4921; fax: +1 901 448 4921. E-mail address: yasun{at}utmem.edu

Heart failure is a global health problem, appearing most commonly in patients with previous myocardial infarction (MI). Cardiac remodelling, particularly fibrosis, seen in both the infarcted and non-infarcted myocardium is recognized to be a major determinant of the development of impaired ventricular function, leading to a poor prognosis. Elucidating cellular and molecular mechanisms responsible for the accumulation of extracellular matrix is essential for designing cardioprotective and reparative strategies that could regress fibrosis after infarction. Multiple factors contribute to left ventricular remodelling at different stages post-MI. This review will discuss the role of oxidative stress and locally produced angiotensin II in the pathogenesis of myocardial repair/remodelling after MI.

KEYWORDS Myocardial infarction; Cardiac remodelling; Oxidative stress; Angiotensin II

Time for primary review: 27 days


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