Calcium Regulation of Vascular Smooth Muscle Cell-Derived Matrix Vesicles
Calcium Regulation of Vascular Smooth Muscle Cell-Derived Matrix Vesicles
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DOI：
10.1016/j.tcm.2012.07.009
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发表时间：
2012-07-01
影响因子：
9.3
通讯作者：
Shanahan, Catherine M.
中科院分区：
文献类型：
--
作者：
Kapustin, Alexander N.;Shanahan, Catherine M.
血管钙化是矿物质代谢紊乱患者常见的病理过程，由血管平滑肌细胞（VSMCs）介导。VSMC钙化起始的一个关键事件是矿化基质囊泡（MV）的释放，这些囊泡是具有使其能够有效地使羟基磷灰石成核的结构特征的小的膜结合体。这些小体类似于骨发育期间软骨细胞分泌的MV，其性质包括不存在钙化抑制剂、成核位点的形成和基质金属蛋白酶如MMP-2的积累。MV生物发生和负载的机制仍然知之甚少;然而，新出现的数据表明，细胞溶质钙稳态的改变可以引发MV组成的多种变化，促进其矿化。（Trends Endovasc Med 2012;22：133-137）（c）2012 Elsevier Inc. All rights reserved.
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. (Trends Cardiovasc Med 2012;22:133-137) (c) 2012 Elsevier Inc. All rights reserved.