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本文引用的文献

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Mechanisms of acute coronary syndromes and their implications for therapy.急性冠状动脉综合征的机制及其对治疗的意义。
N Engl J Med. 2013 May 23;368(21):2004-13. doi: 10.1056/NEJMra1216063.
2
Update on acute coronary syndromes: the pathologists' view.急性冠状动脉综合征的最新进展:病理学家的观点。
Eur Heart J. 2013 Mar;34(10):719-28. doi: 10.1093/eurheartj/ehs411. Epub 2012 Dec 13.
3
A mechanistic analysis of the role of microcalcifications in atherosclerotic plaque stability: potential implications for plaque rupture.微钙化在动脉粥样硬化斑块稳定性中的作用的机制分析:对斑块破裂的潜在影响。
Am J Physiol Heart Circ Physiol. 2012 Sep 1;303(5):H619-28. doi: 10.1152/ajpheart.00036.2012. Epub 2012 Jul 9.
4
Myocardial infarction accelerates atherosclerosis.心肌梗死加速动脉粥样硬化。
Nature. 2012 Jul 19;487(7407):325-9. doi: 10.1038/nature11260.
5
Population trends in the incidence and outcomes of acute myocardial infarction.人口趋势对急性心肌梗死发病率和结局的影响。
N Engl J Med. 2010 Jun 10;362(23):2155-65. doi: 10.1056/NEJMoa0908610.
6
Genetically engineered resistance for MMP collagenases promotes abdominal aortic aneurysm formation in mice infused with angiotensin II.基质金属蛋白酶(MMP)胶原酶的基因工程抗性促进了输注血管紧张素II的小鼠腹主动脉瘤的形成。
Lab Invest. 2009 Mar;89(3):315-26. doi: 10.1038/labinvest.2008.167. Epub 2009 Jan 19.
7
Stabilization of carotid atheroma assessed by quantitative ultrasound analysis in nonhypercholesterolemic patients with coronary artery disease.在非高胆固醇血症冠心病患者中,通过定量超声分析评估颈动脉粥样硬化的稳定性。
J Am Coll Cardiol. 2005 Dec 6;46(11):2022-30. doi: 10.1016/j.jacc.2005.04.070. Epub 2005 Nov 4.
8
Matrix metalloproteinase-13/collagenase-3 deletion promotes collagen accumulation and organization in mouse atherosclerotic plaques.基质金属蛋白酶-13/胶原酶-3缺失促进小鼠动脉粥样硬化斑块中的胶原积累和组织化。
Circulation. 2005 Oct 25;112(17):2708-15. doi: 10.1161/CIRCULATIONAHA.105.562041. Epub 2005 Oct 17.
9
Pathophysiology of coronary artery disease.冠状动脉疾病的病理生理学
Circulation. 2005 Jun 28;111(25):3481-8. doi: 10.1161/CIRCULATIONAHA.105.537878.
10
Spotty calcification typifies the culprit plaque in patients with acute myocardial infarction: an intravascular ultrasound study.斑点状钙化是急性心肌梗死患者罪犯斑块的典型特征:一项血管内超声研究
Circulation. 2004 Nov 30;110(22):3424-9. doi: 10.1161/01.CIR.0000148131.41425.E9. Epub 2004 Nov 22.

胶原酶与斑块中的裂隙。

Collagenases and cracks in the plaque.

机构信息

Division of Cardiovascular Medicine, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

J Clin Invest. 2013 Aug;123(8):3201-3. doi: 10.1172/JCI67526. Epub 2013 Aug 1.

DOI:10.1172/JCI67526
PMID:23908120
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3726161/
Abstract

The core of an atheromatous plaque contains lipids, macrophages, and cellular debris, typically covered by a fibrous cap that separates the thrombogenic core from the blood. Rupture of the fibrous cap causes most fatal myocardial infarctions. Interstitial collagen confers tensile strength on the cap, as it does in skin and tendons. In 1994, Peter Libby and colleagues demonstrated overexpression of collagenolytic enzymes in atheromatous plaques and implicated MMPs in the destabilization of these lesions.

摘要

动脉粥样硬化斑块的核心包含脂质、巨噬细胞和细胞碎片,通常被一层纤维帽覆盖,将血栓形成的核心与血液隔离开来。纤维帽的破裂导致了大多数致命性的心肌梗死。在皮肤和肌腱中,间质胶原赋予帽状结构拉伸强度。1994 年,Peter Libby 及其同事在动脉粥样硬化斑块中证实了胶原酶的过度表达,并表明 MMPs 参与了这些病变的不稳定。