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金属蛋白酶与易损性动脉粥样硬化斑块

Metalloproteinases and vulnerable atherosclerotic plaques.

作者信息

Newby Andrew C

机构信息

University of Bristol, Bristol Heart Institute, Bristol Royal Infirmary, Bristol BS2 8HW.

出版信息

Trends Cardiovasc Med. 2007 Nov;17(8):253-8. doi: 10.1016/j.tcm.2007.09.001.

DOI:10.1016/j.tcm.2007.09.001
PMID:18021934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2850988/
Abstract

Plaque rupture is the main cause of myocardial infarctions and strokes. Ruptured plaques have thin, highly inflamed, and collagen-poor fibrous caps that contain elevated levels of proteases, including metalloproteinases (MMPs), which might weaken plaque caps and promote rupture. On the other hand, MMPs facilitate migration and proliferation vascular smooth muscle cells, which should promote fibrous cap stability. Given the dual effects of MMPs, therapies should selectively target harmful MMPs or the processes that cause MMP activity to rise to destructive levels.

摘要

斑块破裂是心肌梗死和中风的主要原因。破裂的斑块具有薄的、高度发炎且胶原蛋白含量低的纤维帽,其中含有包括金属蛋白酶(MMPs)在内的蛋白酶水平升高,这可能会削弱斑块帽并促进破裂。另一方面,MMPs促进血管平滑肌细胞的迁移和增殖,这应该会促进纤维帽的稳定性。鉴于MMPs的双重作用,治疗应选择性地靶向有害的MMPs或导致MMP活性升至破坏水平的过程。

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