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抑制细胞外基质金属蛋白酶诱导剂可能有助于减少动脉粥样硬化斑块的不稳定性。

Inhibiting extracellular matrix metalloproteinase inducer maybe beneficial for diminishing the atherosclerotic plaque instability.

作者信息

Xie S, Nie R, Wang J

机构信息

Department of Cardiology, The Second Affiliated Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China.

出版信息

J Postgrad Med. 2009 Oct-Dec;55(4):284-6. doi: 10.4103/0022-3859.58936.

DOI:10.4103/0022-3859.58936
PMID:20083879
Abstract

Atherosclerotic plaque rupture and local thrombosis activation in the artery cause acute serious incidents such as acute coronary syndrome and stroke. The exact mechanism of plaque rupture remains unclear but excessive degradation of the extracellular matrix scaffold by matrix-degrading metalloproteinases (MMPs) has been implicated as one of the major molecular mechanisms in this process. Convincing evidence is available to prove that extracellular matrix metalloproteinase inducer (EMMPRIN) induces MMP expression and is involved in the inflammatory responses in the artery wall. The inflammation and MMPs have been shown to play a critical role for atherosclerotic lesion development and progression. More recent data showed that increased EMMPRIN expression was associated with vulnerable atherosclerotic lesions. Therefore, we speculate that EMMPRIN may be pivotal for atherosclerotic plaque instability, and hence inhibition of EMMPRIN expression could be a promising approach for the prevention or treatment of atheroma instability.

摘要

动脉粥样硬化斑块破裂和局部血栓形成激活会引发急性严重事件,如急性冠状动脉综合征和中风。斑块破裂的确切机制尚不清楚,但基质降解金属蛋白酶(MMPs)对细胞外基质支架的过度降解被认为是这一过程中的主要分子机制之一。有确凿证据证明细胞外基质金属蛋白酶诱导剂(EMMPRIN)可诱导MMP表达,并参与动脉壁的炎症反应。炎症和MMPs已被证明在动脉粥样硬化病变的发展和进展中起关键作用。最近的数据表明,EMMPRIN表达增加与易损性动脉粥样硬化病变相关。因此,我们推测EMMPRIN可能对动脉粥样硬化斑块的不稳定性起关键作用,因此抑制EMMPRIN表达可能是预防或治疗动脉粥样硬化不稳定的一种有前景的方法。

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