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Review
. 2009 Feb 15;81(3):482-90.
doi: 10.1093/cvr/cvn333. Epub 2008 Dec 2.

Myocardial repair/remodelling following infarction: roles of local factors

Yao Sun  1
Affiliations
Review

Myocardial repair/remodelling following infarction: roles of local factors

Yao Sun. Cardiovasc Res. .

Abstract

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.

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Figures

Figure 1
Figure 1
NADPH oxidase (gp91phox) expression in the infarcted rat heart. Detected by in situ hybridization, low levels of gp91phox mRNA are present in both left and right ventricles (LV, RV) of the normal heart (A). At 1 week post-myocardial infarction, cardiac gp91phox mRNA levels are largely increased, particularly at the site of myocardial infarction (B). Detected by western blot, gp91phox protein levels are significantly increased in the infarcted myocardium compared with the normal myocardium (C). Immunohistochemistry reveals that cells expressing gp91phox in the infarcted myocardium are primarily inflammatory cells (D).
Figure 2
Figure 2
Expression of superoxide dismutase, malondialdehyde, and 3-nitrotyrosine in the infarcted rat heart. At 1 week post-myocardial infarction, superoxide dismutase mRNA (A) and protein (B) levels are significantly reduced in the infarcted myocardium. Compared with normal heart, malondialdehyde levels are significantly increased in the infarcted myocardium (C). 3-Nitrotyrosine is highly expressed by inflammatory cells at the infarct site (D).
Figure 3
Figure 3
Transforming growth factor-β1, angiotensin-converting enzyme, and AT1 receptor expression in the infarcted heart. By in situ hybridization, normal myocardium contains low levels of Transforming growth factor-β1 (A). At week 1 post-myocardial infarction, Transforming growth factor-β1 gene expression is largely increased at the site of myocardial infarction (B). Detected by autoradiography, binding density of angiotensin-converting enzyme (D) and AT1 receptors (F) are largely increased in both the infarcted and non-infarcted myocardium compared with the normal heart (C and E, respectively).
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