Parhami F, Tintut Y, Patel J K, Mody N, Hemmat A, Demer L L
Division of Cardiology, UCLA School of Medicine, Center for the Health Sciences, 47-123, 10833 Le Conte Avenue, Los Angeles, CA 90095, USA.
Z Kardiol. 2001;90 Suppl 3:27-30. doi: 10.1007/s003920170038.
Over a century ago it was recognized that the vessel wall is a predominant site for ectopic calcification which is a hallmark of clinically significant atherosclerotic lesions. Old observational studies, which characterized vascular calcification as osteogenesis, and recent identification of common molecular mechanisms in bone and vascular calcification have led to the new recognition that atherosclerotic calcification is an actively regulated process similar to osteogenesis and distinct from a metastatic passive mineralization. Since the atherosclerotic lesion is composed of a multitude of cells and inflammatory mediators, elucidation of the role of these components in induction and acceleration of calcification is of fundamental importance in better understanding its pathogenesis and identifying possible interventional targets. This article will focus on four important mediators of vascular calcification: 1) calcifying vascular cells, 2) oxidized lipids, 3) cytokines, and 4) leptin.
一个多世纪以前,人们就认识到血管壁是异位钙化的主要部位,而异位钙化是临床上显著的动脉粥样硬化病变的一个标志。过去的观察性研究将血管钙化描述为骨生成,以及最近在骨和血管钙化中发现的共同分子机制,促使人们重新认识到动脉粥样硬化钙化是一个类似于骨生成的、受积极调控的过程,不同于转移性被动矿化。由于动脉粥样硬化病变由多种细胞和炎症介质组成,阐明这些成分在钙化诱导和加速中的作用,对于更好地理解其发病机制和确定可能的干预靶点至关重要。本文将聚焦于血管钙化的四种重要介质:1)钙化血管细胞,2)氧化脂质,3)细胞因子,以及4)瘦素。