Lijnen H Roger
Center for Molecular and Vascular Biology, KU Leuven, Belgium.
Pathophysiol Haemost Thromb. 2003;33(5-6):275-81. doi: 10.1159/000083814.
Remodeling of the vascular wall plays a role in many physiological processes, but also in the pathogenesis of major cardiovascular diseases such as restenosis and atherosclerosis. Remodeling requires proteolytic activity to degrade components of the extracellular matrix; this can be generated by the matrix metalloproteinase(MMP) system alone or in concert with the fibrinolytic (plasminogen/plasmin) system. Several lines of evidence suggest that the MMP system plays a role in vascular smooth muscle cell migration and neointima formation after vascular injury. In atherosclerotic lesions, active MMPs may contribute to plaque destabilisation by degrading extracellular matrix components, but may also promote aneurysm formation by proteolytic degradation of the elastic lamina. The MMP system may therefore represent a potential therapeutic target for treatment of restenosis or atherosclerosis.
血管壁重塑在许多生理过程中发挥作用,在诸如再狭窄和动脉粥样硬化等主要心血管疾病的发病机制中也发挥作用。重塑需要蛋白水解活性来降解细胞外基质的成分;这可以仅由基质金属蛋白酶(MMP)系统产生,或与纤维蛋白溶解(纤溶酶原/纤溶酶)系统协同产生。几条证据线索表明,MMP系统在血管损伤后血管平滑肌细胞迁移和新生内膜形成中发挥作用。在动脉粥样硬化病变中,活性MMP可能通过降解细胞外基质成分导致斑块不稳定,但也可能通过对弹性膜的蛋白水解降解促进动脉瘤形成。因此,MMP系统可能是治疗再狭窄或动脉粥样硬化的潜在治疗靶点。