中文摘要：

血管钙化是由于高钙磷环境以及局部或全身矿化诱导子上调、抑制子下调所导致的骨特异性羟基磷灰石结晶主动沉积在血管壁的病理过程。在这一过程中,血管壁矿化防御机制被耗竭,平滑肌细胞等间叶细胞丢失原有表型而获得成骨表型,释放矿化脂质小泡。脂质小泡（在动脉壁至少存在基质小泡和凋亡小体两种形式）为钙化结晶提供了合适的成核微环境,而血管壁弹性蛋白则为羟基磷灰石沉积提供了支架结构。因此在钙沉积（成骨细胞样细胞介导）与钙吸收（破骨细胞样细胞介导）之间的平衡被打破后,血管壁内膜、中膜或主动脉瓣膜就可能形成异位钙化。针对钙化形成的机制及钙化危险因素进行干预和调控,有可能对血管钙化的逆转和消退带来有益的影响,尤其是对钙化灶内破骨细胞或破骨细胞样细胞数量与活性的上调可能是一个更有效的治疗策略。但由于骨-血管轴钙化异象的存在,如何将正位骨形成与异位钙吸收有机的协调在一起尚是今后研究的一个难题。

英文摘要：

Vascular calcification is an active,cell-regulated process,characterized by the deposition of hydroxyapatite crystal in vascular wall,resulted from high-calcium/phosphate-environment,up-regulation of mineralization inducers and down-regulation of mineralization inhibitor in local or systemic sites.In this process,the protective system against vascular mineralization is exhausted,and mesenchyma,such as vascular smooth muscle cells（VSMC）,lose the intrinsic phenotypes,but gain the osteogenic phenotypes.Consequently,mineralized cells release some lipid vesicles,which have two forms at least in vascular wall,such as matrix vesicle and apoptosis body.Lipid vesicles provide appropriate nucleating micro-environments for vascular calcification,and vascular elastin provides the bracket structure for hydroxyapatite deposition.So,under the condition that the balance between calcium deposition（mediated by osteoblast-like cells）and calcium absorption（mediated by osteoclast-like cells）is disrupted,ectopic calcification of vascular intima,media or aortic valve may be developed.Intervention on the mechanisms and risk factors of vascular calcification may bring some beneficial effects on the reverse and regression of vascular calcification.In particular,up-regulation on the number and activity of osteoclasts or osteoclast-like cells in calcification lesion may be a more efficient therapeutic strategy.However,it will be a difficult problem in future how to coordinate the relation between normotopic bone formation and ectopic calcification absorption because of calcification paradox in bone-vascular axis.