Role of matrix metalloproteinase-8 in atherosclerosis.

Role of matrix metalloproteinase-8 in atherosclerosis.
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DOI:
10.1155/2013/659282
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发表时间:
2013
影响因子:
4.6
通讯作者:
Montecucco F
Montecucco F
中科院分区:
医学3区
文献类型:
--
作者:
Lenglet S;Mach F;Montecucco F

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斑块破裂是急性心肌梗死和脑卒中的主要原因。当动脉粥样硬化斑块的特征为薄的、高度发炎的和胶原蛋白贫乏的纤维帽并且含有升高水平的蛋白酶(包括金属蛋白酶(MMP))时,动脉粥样硬化斑块被描述为是脆弱的并且更容易破裂。斑块中胶原分解的起始需要间质胶原酶,即由MMP-1、MMP-8和MMP-13组成的MMP亚家族。以往的研究表明,MMP-1和MMP-13在人和实验性动脉粥样硬化中均可能过表达。由于嗜中性粒细胞最近才被报道在动脉粥样硬化斑块中,MMP-8(以前称为“嗜中性粒细胞胶原酶”)的作用仅被边缘评价。在本文中,我们将更新和评论的证据,最相关的调节途径和活动介导的MMP-8在动脉粥样硬化形成。
Plaque rupture is the main cause of acute myocardial infarction and stroke. Atherosclerotic plaques have been described to be vulnerable and more prone to rupture when they are characterized by thin, highly inflamed, and collagen-poor fibrous caps and contain elevated levels of proteases, including metalloproteinases (MMPs). Initiation of collagen breakdown in plaques requires interstitial collagenases, a MMP subfamily consisting of MMP-1, MMP-8, and MMP-13. Previous reports demonstrated that MMP-1 and MMP-13 might be overexpressed in both human and experimental atherosclerosis. Since neutrophils have been only recently reported in atherosclerotic plaques, the role of MMP-8 (formerly known as “neutrophil collagenase”) was only marginally evaluated. In this paper, we will update and comment on evidence of the most relevant regulatory pathways and activities mediated by MMP-8 in atherogenesis.
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发表时间: 1994-12-01
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