Key result
Matrix metalloproteinases drive progressive post-MI myocardial remodeling, plaque rupture, and aortic aneurysm formation.
Why the study?
Matrix metalloproteinases have been demonstrated to cause tissue remodeling, but their contributory role in cardiovascular remodeling requires comprehensive examination.
This review highlights the critical pathophysiological role of matrix metalloproteinases in driving adverse cardiovascular remodeling across various conditions including post-MI heart failure, atherosclerosis, and aortic aneurysms.
May inform MMP inhibitor development for remodeling; leaves open clinical utility pending prospective trials.
Changes in cardiovascular tissue structure can result in alterations in function. This process occurs as a continuum and can be defined as cardiovascular remodeling. A family of zinc dependent proteases known as the matrix metalloproteinases (MMPs) has been demonstrated to cause tissue remodeling. A number of past studies have demonstrated increased expression and activation of MMPs in both myocardial and vascular remodeling processes. Experimental results support the concept that the MMPs directly contribute to progressive myocardial remodeling post-myocardial infarction and in cardiomyopathic disease. Within the vascular compartment, compelling evidence exists for the contributory role of MMPs in atheromatous plaque rupture and aortic aneurysms. Therefore, the purpose of this review is to examine recent studies of this proteolytic system in the context of cardiovascular remodeling.
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Gunasinghe et al. (2001) conducted a review in Cardiovascular remodeling. Matrix metalloproteinases (MMPs) was evaluated. Matrix metalloproteinases (MMPs) contribute to progressive myocardial remodeling post-myocardial infarction, cardiomyopathic disease, atheromatous plaque rupture, and aortic aneurysms.
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