© 2002 by European Society of Cardiology
Copyright © 2002, European Society of Cardiology
Matrix metalloproteinase-9 expression after myocardial infarction: physiological or pathological?
aDepartment of Surgery, University of Leicester, Leicester, UK
bDepartment of Medicine and Therapeutics, University of Leicester, Leicester, UK
mattt11@aol.com
* Corresponding author. Department of Surgery, RKCSB, Leicester Royal Infirmary, Leicester, LE2 7LX UK. Tel.: +44-11-6252-3252; fax: +44-11-6252-3179
Received 18 March 2002; accepted 18 March 2002
| The first 150 words of the full text of this article appear below. |
See article by Romanic et al. [24] (pages 549–558) in this issue.
Remodelling of the extracellular matrix is acknowledged to play a significant role in a number of vascular disorders including aneurysm formation, rupture of atherosclerotic plaques, and development of intimal hyperplasia [1,2]. In recent years, investigations of matrix biology have been applied to cardiac remodelling following acute myocardial infarction (MI). Left ventricular dilatation following MI is related to the extent of the ischaemic insult and subsequent healing of the infarct and surrounding tissue [3]. Whilst the process of postinfarct remodelling is incompletely understood, excessive degradation of extracellular matrix components appears to result in pathological cardiac remodelling, left ventricular dilatation and cardiac failure.
The major physiological regulators of the extracellular matrix are the matrix metalloproteinases (MMP), which have been implicated in the genesis of postinfarct ventricular failure [6]. The MMPs are a family of structurally related endopeptidases
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1 Expression of MMPs following MI |
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2 Ventricular remodelling and MMP expression |
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3 Myocardial infarction and MMP-9 |
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4 Clinical observations |
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