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Keywords
Matrix metalloproteinases; Tissue inhibitors of matrix metalloproteinases; Myocardial infarction; Myocardial remodeling; Fibronectin; Angiotensin II receptor blockade; Valsartan
Introduction
It has been well-documented that angiotensin II (Ang II) type 1 (AT1) receptor blocker (ARB) can attenuate myocardial remodeling and preserve cardiac function in infarcted Idelalisib [11]. However, the underlying mechanism remands elusive. The stimulatory role of Ang II in the activity of MMPs has been recognized recently [12]. Therefore, it is likely that the beneficial effect of ARB on myocardial remodeling is attributed to its inhibitory property on Ang II-induced MMPs activation.
Fibronectin (FN) is a major component of ECM [13]. Break down of FN by MMPs will facilitate myocardial remodeling [14]. The present study was designed to determine whether MI is associated with an imbalance between myocardial MMPs (MMP-2, MMP-3 and MMP-9) and TIMP-1 and a change in FN level, and whether Ang II receptor blockade could normalize the MMPs/TIMP-1 balance and restore the expression level of FN in rat infarcted myocardium.