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动脉粥样硬化中的钙化:动脉交叉点处的骨生物学与慢性炎症

Calcification in atherosclerosis: bone biology and chronic inflammation at the arterial crossroads.

作者信息

Doherty Terence M, Asotra Kamlesh, Fitzpatrick Lorraine A, Qiao Jian-Hua, Wilkin Douglas J, Detrano Robert C, Dunstan Colin R, Shah Prediman K, Rajavashisth Tripathi B

机构信息

Atherosclerosis Research Center and the Burns and Allen Research Institute, Division of Cardiology, Department of Medicine, Cedars-Sinai Medical Center and David Geffen School of Medicine, University of California, Los Angeles, CA 90048, USA.

出版信息

Proc Natl Acad Sci U S A. 2003 Sep 30;100(20):11201-6. doi: 10.1073/pnas.1932554100. Epub 2003 Sep 19.

Abstract

Dystrophic or ectopic mineral deposition occurs in many pathologic conditions, including atherosclerosis. Calcium mineral deposits that frequently accompany atherosclerosis are readily quantifiable radiographically, serve as a surrogate marker for the disease, and predict a higher risk of myocardial infarction and death. Accelerating research interest has been propelled by a clear need to understand how plaque structure, composition, and stability lead to devastating cardiovascular events. In atherosclerotic plaque, accumulating evidence is consistent with the notion that calcification involves the participation of arterial osteoblasts and osteoclasts. Here we summarize current models of intimal arterial plaque calcification and highlight intriguing questions that require further investigation. Because atherosclerosis is a chronic vascular inflammation, we propose that arterial plaque calcification is best conceptualized as a convergence of bone biology with vascular inflammatory pathobiology.

摘要

营养不良性或异位性矿物质沉积发生于许多病理状况中,包括动脉粥样硬化。常伴随动脉粥样硬化出现的钙矿物质沉积可通过影像学轻易定量,作为该疾病的替代标志物,并预示着更高的心肌梗死和死亡风险。由于明确需要了解斑块结构、组成和稳定性如何导致毁灭性心血管事件,研究兴趣日益浓厚。在动脉粥样硬化斑块中,越来越多的证据支持钙化涉及动脉成骨细胞和破骨细胞参与的观点。在此,我们总结内膜动脉斑块钙化的当前模型,并突出需要进一步研究的有趣问题。鉴于动脉粥样硬化是一种慢性血管炎症,我们提出动脉斑块钙化最好被理解为骨生物学与血管炎性病理生物学的融合。

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