Cadherin:catenin complex:: A novel regulator of vascular smooth muscle cell behaviour
Cadherin:catenin complex:: A novel regulator of vascular smooth muscle cell behaviour
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DOI：
10.1016/j.atherosclerosis.2005.12.017
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发表时间：
2006-09-01
期刊：
影响因子：
5.3
通讯作者：
Beeching, C. A.
中科院分区：
文献类型：
--
作者：
George, S. J.;Beeching, C. A.
功能障碍的血管平滑肌细胞(VSMC)行为参与了动脉粥样硬化和再狭窄的发病机制。VSMC凋亡率的增加被认为导致纤维性动脉粥样硬化斑块变薄，从而导致不稳定，而VSMC向内膜的迁移和不适当的VSMC增殖，导致动脉粥样硬化和再狭窄时发生的内膜增厚。主要是在癌症和神经细胞中的研究表明，细胞与细胞之间的黏附通过钙粘蛋白：连环蛋白复合体调节细胞的凋亡、迁移和增殖。相比之下，直到最近，这种复合体参与VSMC行为调控的研究还相对较少。在这篇综述中，我们将讨论钙粘蛋白：连环蛋白复合体对VSMC凋亡、迁移和增殖调控的证据。(C)2005爱思唯尔爱尔兰有限公司。保留所有权利。
Dysfunctional vascular smooth muscle cell (VSMC) behaviour contributes to the pathogenesis of atherosclerosis and restenosis. Increased rates of VSMC apoptosis are thought to lead to thinning of the fibrous atherosclerotic plaque and thereby instability, while migration of VSMCs to the intima, and inappropriate VSMC proliferation, contribute to intimal thickening that occurs in atherosclerosis and restenosis. Studies, mainly in cancer and neuronal cells, have demonstrated that cell-cell adhesion by the cadherin:catenin complex modulates apoptosis, migration and proliferation. In contrast, until recently the involvement of this complex in the regulation of VSMC behaviour was relatively unstudied. In this review, evidence for the regulation of VSMC apoptosis, migration and proliferation by the cadherin:catenin complex will be discussed. (c) 2005 Elsevier Ireland Ltd. All rights reserved.