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Osteogenic regulation of vascular calcification:an early perspective
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发表状态：
Am J Physiol Endocrinol Metab 286: E686–E696, ;
研究团队：
Radhika Vattikuti and Dwight A. Towler
研究内容：
动脉粥样硬化(纤维化)钙化、心脏瓣膜钙化、内动脉钙化和血管钙化至少有四种组织解剖学变异，是对代谢、机械、感染和炎症损伤的反应。前三种变异的共同特点是T细胞和巨噬细胞的血管浸润程度不同。钙化性血管病变曾被认为是良性的，但其有害的临床后果现在变得越来越明显。本文简要回顾了血管钙化病理生物学中出现的一些新主题，并强调了我们对血管内分泌学和代谢的理解中存在的一些与人类健康和保健直接相关的基本缺陷。
Abstract：
Cardiovascular calcification is a common consequence of aging, diabetes, hypercholesterolemia, mechanically abnormal valve function, and chronic renal insufficiency. Although vascular calcification may appear to be a uniform response to vascular insult, it is a heterogenous disorder, with overlapping yet distinct mechanisms of initiation and progression. A minimum of four histoanatomic variants—atherosclerotic (fibrotic) calcification, cardiac valve calcification, medial artery calcification, and vascular calciphylaxis—arise in response to metabolic, mechanical, infectious, and inflammatory injuries. Common to the first three variants is a variable degree of vascular infiltration by T cells and macrophages. Once thought benign, the deleterious clinical consequences of calcific vasculopathy are now becoming clear; stroke, amputation, ischemic heart disease, and increased mortality are portended by the anatomy and extent of calcific vasculopathy. Along with dystrophic calcium deposition in dying cells and lipoprotein deposits, active endochondral and intramembranous (nonendochondral) ossification processes contribute to vascular calcium load. Thus vascular calcification is subject to regulation by osteotropic hormones and skeletal morphogens in addition to key inhibitors of passive tissue mineralization. In response to oxidized lipids, inflammation, and mechanical injury, the microvascular smooth muscle cell becomes activated. Orthotopically, proliferating stromal myofibroblasts provide osteoprogenitors for skeletal growth and fracture repair; however, in valves and arteries, vascular myofibroblasts contribute to cardiovascular ossification. Current >
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