Demer Linda L, Tintut Yin
Department of Medicine, The David Geffen School of Medicine at University of California Los Angeles, 90095-1679, USA.
Arterioscler Thromb Vasc Biol. 2003 Oct 1;23(10):1739-43. doi: 10.1161/01.ATV.0000093547.63630.0F. Epub 2003 Sep 4.
Research in the area of vascular calcification has grown rapidly in the past decade, and there is a greater understanding of its active regulatory mechanisms. This brief review covers the ideas presented in the 2003 Jeffrey M. Hoeg Award lecture, including the concepts that bone tissue forms in the artery wall in patients with atherosclerosis, that vascular cells undergo osteoblastic differentiation, that bone morphogenetic protein and matrix GLA protein regulate vascular calcification in opposition, that inflammatory cytokines and lipids promote vascular cell calcification but inhibit osteoblastic cell differentiation, that these same factors promote differentiation of bone-resorbing osteoclasts, and that the artery wall may contain osteoclast-like cells with the potential to resorb calcium mineral. The review closes with a mention of therapeutic possibilities and an evolutionary paradigm to explain the reciprocal responses of vascular and bone mineralization to inflammation.
在过去十年中，血管钙化领域的研究迅速发展，人们对其活跃的调控机制有了更深入的了解。这篇简短的综述涵盖了2003年杰弗里·M·霍格奖讲座中提出的观点，包括动脉粥样硬化患者动脉壁中形成骨组织的概念、血管细胞经历成骨细胞分化的概念、骨形态发生蛋白和基质GLA蛋白对血管钙化起相反调节作用的概念、炎性细胞因子和脂质促进血管细胞钙化但抑制成骨细胞分化的概念、这些相同因素促进骨吸收破骨细胞分化的概念，以及动脉壁可能含有具有吸收钙矿物质潜力的破骨细胞样细胞的概念。综述最后提到了治疗可能性以及一种进化范式，以解释血管和骨矿化对炎症的相互反应。
