基质金属蛋白酶
纤维帽
炎症
巨噬细胞
免疫系统
先天免疫系统
易损斑块
心肌梗塞
医学
不稳定型心绞痛
免疫学
基因剔除小鼠
生物
病理
受体
心脏病学
内科学
体外
生物化学
作者
Juntang Lin,Vijay V. Kakkar,Xinjie Lu
标识
DOI:10.2174/1389450115666140211115805
摘要
Atherosclerosis is now widely recognized as a chronic inflammatory disease that involves innate and adaptive immune responses. Both cellular and humoral components of the immune system have been implicated in atherogenesis. Growing evidence suggests that immune cells play crucial roles in atherogenic plaque formation. Vulnerability of the plaque probably plays an important role in rupture. Most ruptures occur at the periphery of the fibrous cap that covers the lipid-rich core-points where the cap is usually thinnest and most heavily infiltrated by macrophage foam cells. Sudden rupture of a plaque triggers unstable angina, acute myocardial infarction, and sudden cardiac death. Initiation of collagen breakdown in plaques requires matrix metalloproteinase (MMP) family members including MMP-1, MMP-8, and MMP- 13. In addition, other MMPs such as MMP-2, -3, -9, -10 and -12 have also been reported to play roles in atherosclerosis. This review aims to focus on description of general structural features of MMPs and their roles in atherosclerosis.
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