Division of Cardiology, David Geffen School of Medicine, University of California, Los Angeles, Center for the Health Sciences, A2-237, 10833 Le Conte Ave., Los Angeles, CA, 90095-1679, USA.
Cell Mol Life Sci. 2013 Sep;70(17):3187-97. doi: 10.1007/s00018-012-1231-y. Epub 2012 Dec 27.
Vascular calcification is a common feature of chronic kidney disease, cardiovascular disease, and aging. Such abnormal calcium deposition occurs in medial and/or intimal layers of blood vessels as well as in cardiac valves. Once considered a passive and inconsequential finding, the presence of calcium deposits in the vasculature is widely accepted as a predictor of increased morbidity and mortality. Recognition of the importance of vascular calcification in health is driving research into mechanisms that govern its development, progression, and regression. Diverse, but highly interconnected factors, have been implicated, including disturbances in lipid metabolism, oxidative stress, inflammatory cytokines, and mineral and hormonal balances, which can lead to formation of osteoblast-like cells in the artery wall. A tight balance of procalcific and anticalcific regulators dictates the extent of disease. In this review, we focus on the main regulatory circuits modulating vascular cell calcification.
血管钙化是慢性肾脏病、心血管疾病和衰老的共同特征。这种异常的钙沉积发生在血管的中膜和/或内膜层以及心脏瓣膜中。血管中钙沉积的存在曾被认为是一种被动且无关紧要的发现,但现在已被广泛认为是发病率和死亡率增加的预测因素。对血管钙化在健康中的重要性的认识,推动了对其发生、发展和消退机制的研究。包括脂质代谢紊乱、氧化应激、炎性细胞因子以及矿物质和激素平衡在内的多种相互关联的因素已被牵涉其中,这些因素可能导致动脉壁中出现成骨样细胞。促钙化和抗钙化调节剂之间的紧密平衡决定了疾病的严重程度。在这篇综述中,我们重点关注调节血管细胞钙化的主要调节回路。