BHF Centre of Research Excellence, Cardiovascular Division, King's College London, London SE5 9NU, UK.
Trends Cardiovasc Med. 2012 Jul;22(5):133-7. doi: 10.1016/j.tcm.2012.07.009. Epub 2012 Aug 16.
Vascular calcification is a pathological process common in patients with disorders of mineral metabolism and mediated by vascular smooth muscle cells (VSMCs). A key event in the initiation of VSMC calcification is the release of mineralization-competent matrix vesicles (MVs), small membrane-bound bodies with structural features enabling them to efficiently nucleate hydroxyapatite. These bodies are similar to MVs secreted by chondrocytes during bone development and their properties include the absence of calcification inhibitors, formation of nucleation sites, and accumulation of matrix metalloproteinases such as MMP-2. The mechanisms of MV biogenesis and loading remain poorly understood; however, emerging data have demonstrated that alterations in cytosolic calcium homeostasis can trigger multiple changes in MV composition that promote their mineralization.
血管钙化是矿物质代谢紊乱患者中常见的病理过程，由血管平滑肌细胞（VSMCs）介导。VSMC 钙化启动的关键事件是释放具有矿化能力的基质小泡（MVs），这些小泡是带有结构特征的小型膜结合体，能够有效地成核羟基磷灰石。这些小泡类似于软骨细胞在骨骼发育过程中分泌的 MVs，其特性包括缺乏钙化抑制剂、形成成核位点以及积累基质金属蛋白酶（如 MMP-2）。MV 生物发生和加载的机制仍知之甚少；然而，新出现的数据表明，细胞溶质钙稳态的改变可以触发 MV 组成的多种变化，从而促进其矿化。
