Liu Peter, Sun Mei, Sader Sawsan
Heart & Stroke/Richard Lewar Centre of Excellence, and the Department of Physiology, Toronto General Hospital, Toronto, Ontario.
Can J Cardiol. 2006 Feb;22 Suppl B(Suppl B):25B-30B. doi: 10.1016/s0828-282x(06)70983-7.
Matrix metalloproteinases (MMPs) are a family of proteolytic enzymes that are regulated by inflammatory signals to mediate changes in extracellular matrix. Members of the MMP family share sequence homology, act on interstitial protein substrates, acutely participate in inflammatory processes and chronically mediate tissue remodelling. MMPs are important in vascular remodelling, not only in the overall vasculature architecture but also, more importantly, in the advancing atherosclerotic plaque. MMP activation modifies the architecture of the plaque and may directly participate in the process of plaque rupture. MMPs also participate in cardiac remodelling following myocardial infarction and development of dilated cardiomyopathy. Soluble MMPs are now potential biomarkers in delineating cardiovascular risk for plaque rupture and coronary risk. They also constitute innovative direct or indirect targets to modify cardiovascular tissue remodelling in atherosclerosis and heart failure.
基质金属蛋白酶(MMPs)是一类蛋白水解酶家族,受炎症信号调节,介导细胞外基质的变化。MMP家族成员具有序列同源性,作用于间质蛋白底物,急性参与炎症过程,慢性介导组织重塑。MMPs在血管重塑中很重要,不仅在整体血管结构中,更重要的是在进展性动脉粥样硬化斑块中。MMP激活会改变斑块结构,并可能直接参与斑块破裂过程。MMPs还参与心肌梗死后的心脏重塑和扩张型心肌病的发展。可溶性MMPs现在是描绘斑块破裂心血管风险和冠状动脉风险的潜在生物标志物。它们也是改变动脉粥样硬化和心力衰竭中心血管组织重塑的创新直接或间接靶点。