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首页> 外文期刊>Current opinion in lipidology >Do metalloproteinases destabilize vulnerable atherosclerotic plaques?
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Do metalloproteinases destabilize vulnerable atherosclerotic plaques?

机译：金属蛋白酶会破坏脆弱的动脉粥样硬化斑块吗？

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PURPOSE OF REVIEW: Atherosclerotic plaque rupture and thrombosis underlie most myocardial infarctions. Matrix metalloproteinases are a family of enzymes that remodel the extracellular matrix. Metalloproteinases could stabilize rupture-prone plaques by promoting smooth muscle cell migration and proliferation. Alternatively, metalloproteinases could destabilize vulnerable plaques by promoting matrix destruction, angiogenesis, leucocyte infiltration, and apoptosis. Evidence is reviewed from genetically modified mice and human biomarker and genetic studies that sheds light on this dual role of metalloproteinases. RECENT FINDINGS: Inhibition of metalloproteinases in mice using tissue inhibitors of metalloproteinases increases plaque stability; however, double knockouts of apolipoprotein E with matrix metalloproteinase 2, 3, 7, 9, 12, and 13 have more or less stable plaques, consistent with harmful or protective effects of individual metalloproteinases. Overexpression studies in mice or rabbits show that high activities of matrix metalloproteinase 9 and 12 decrease stability. Biomarker and human genetic studies demonstrate that increased metalloproteinase activity is associated with vascular repair or myocardial infarction. SUMMARY: Recent studies reinforce evidence for a dual role of matrix metalloproteinases in plaque stabilization and rupture, which probably depends on the stage, site, and severity of disease. Dysregulated metalloproteinase activity in end-stage coronary artery disease appears a valid target for therapy.
机译：审查目的：动脉粥样硬化斑块破裂和血栓形成是大多数心肌梗塞的基础。基质金属蛋白酶是重塑细胞外基质的一族酶。金属蛋白酶可以通过促进平滑肌细胞迁移和增殖来稳定易破裂斑块。或者，金属蛋白酶可通过促进基质破坏，血管生成，白细胞浸润和凋亡来破坏易损斑块的稳定性。综述了转基因小鼠和人类生物标志物以及遗传研究的证据，这些证据揭示了金属蛋白酶的双重作用。最新发现：使用金属蛋白酶组织抑制剂抑制小鼠中的金属蛋白酶可增加菌斑的稳定性。然而，用基质金属蛋白酶2、3、7、9、12和13双重剔除载脂蛋白E具有或多或少的稳定噬菌斑，这与单个金属蛋白酶的有害或保护作用一致。在小鼠或兔子中的过表达研究表明，基质金属蛋白酶9和12的高活性降低了稳定性。生物标志物和人类遗传学研究表明，金属蛋白酶活性增加与血管修复或心肌梗塞有关。摘要：最近的研究加强了基质金属蛋白酶在斑块稳定和破裂中的双重作用的证据，这可能取决于疾病的阶段，部位和严重程度。终末期冠状动脉疾病中金属蛋白酶活性失调似乎是治疗的有效靶点。

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