Dellegrottaglie S, Sanz J, Rajagopalan S
The Zena and Michael A. Wiener Cardiovascular Institute and The Marie-Josée and Henry R. Kravis Center for Cardiovascular Health, The Mount Sinai Medical Center, New York, NY 10029, USA.
Curr Mol Med. 2006 Aug;6(5):515-24. doi: 10.2174/156652406778018653.
Vascular calcification (VC) is an orchestrated event, evoking the programmed process of the osteogenesis and triggered by inflammatory cytokines active at vascular level. VC is a dynamic process in which the vessel wall intima, media and also cardiac valves may be involved. Intimal calcification is an endochondral ossification process in which type II collagen is mineralized by calcium deposition. In contrast, an intra-membranous ossification process leads to medial calcification, while a dystrophic calcification process is responsible for valvular calcification. Mechanisms involved in VC may be summarized as: 1. Activation of osteogenesis in the vessel wall, 2. Loss of inhibitory factors, 3. Enhanced bone turnover, and 4. Abnormalities in mineral metabolism. The signaling axis constituted by osteoprotegerin (OPG), receptor activator nuclear factor kB (RANK) and its ligand (RANKL), along with the monocyte colony stimulating factor (M-CSF) and the transcription factor core Binding protein (Cbfa-1), play a pivotal role in the control of VC. In contrast, fetuin-A, matrix G1a protein (MGP) and osteopontin (OPN) control the inhibition of VC. In addition, abnormal mineral metabolism with enhanced phosphates availability favors calcium deposition. The inflammatory cytokines interleukin (IL-1) and tumor necrosis factor (TNF)-alpha enhance OPG and RANKL function in the vessel wall leading to VC. VC is a controlled process, depending on the balance between osteoblastic and osteoclastic influences and further modulated by the influence of risk factors like diabetes, smoking, age, hypertension and dyslipidemia. Recent advances in diagnostic tools such as with multi-detector computed tomography (MDCT) and electron beam computed tomography (EBCT), may help diagnosis and delineation of VC in the clinical setting and aid in understanding its prognostic value.
血管钙化（VC）是一个精心编排的过程，引发成骨的程序性进程，并由血管水平活跃的炎性细胞因子触发。VC是一个动态过程，血管壁内膜、中膜以及心脏瓣膜都可能参与其中。内膜钙化是一个软骨内成骨过程，其中II型胶原通过钙沉积而矿化。相比之下，膜内成骨过程导致中膜钙化，而营养不良性钙化过程则导致瓣膜钙化。VC涉及的机制可概括为：1. 血管壁成骨的激活；2. 抑制因子的丧失；3. 骨转换增强；4. 矿物质代谢异常。由骨保护素（OPG）、核因子κB受体激活剂（RANK）及其配体（RANKL），以及单核细胞集落刺激因子（M-CSF）和转录因子核心结合蛋白（Cbfa-1）构成的信号轴，在VC的控制中起关键作用。相比之下，胎球蛋白-A、基质G1a蛋白（MGP）和骨桥蛋白（OPN）控制着对VC的抑制。此外，磷酸盐可用性增加导致的矿物质代谢异常有利于钙沉积。炎性细胞因子白细胞介素（IL-1）和肿瘤坏死因子（TNF）-α增强血管壁中OPG和RANKL的功能，导致VC。VC是一个受控制的过程，取决于成骨细胞和破骨细胞影响之间的平衡，并进一步受到糖尿病、吸烟、年龄、高血压和血脂异常等危险因素的影响而调节。多排探测器计算机断层扫描（MDCT）和电子束计算机断层扫描（EBCT）等诊断工具的最新进展，可能有助于在临床环境中诊断和描绘VC，并有助于理解其预后价值。
