Progenitor cell-derived smooth muscle cells in vascular disease
Progenitor cell-derived smooth muscle cells in vascular disease
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DOI：
10.1016/j.bcp.2010.01.027
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发表时间：
2010-06-15
影响因子：
5.8
通讯作者：
Bennett, Martin
中科院分区：
文献类型：
--
作者：
Orlandi, Augusto;Bennett, Martin
血管平滑肌细胞（VSMCs）在血管内图尼卡内膜中的积聚在动脉粥样硬化和血管内手术后再狭窄的发病机制中起主要作用。动脉VSMCs即使在正常血管壁中也是异质的，并且在生理和病理条件下显示不同的表型。在经典范例中，血管壁损伤诱导VSMC去分化、增殖和响应于生长因子和蛋白水解剂从中膜迁移到内膜。因此，动脉粥样硬化斑块和再狭窄中的VSMC与正常介质中的“收缩”表型相比显示去分化或“合成”表型。相反，最近的研究已经确定了骨髓和外周血来源的内皮和VSMC祖细胞，可能有助于动脉粥样硬化，动脉损伤后和移植动脉粥样硬化内膜形成。这些骨髓来源的血管前体细胞的确切频率是有争议的，它们的作用是未知的。此外，额外的数据支持存在常驻祖细胞亚群，并参与成人动脉壁对损伤或缺血的反应。这篇综述将研究祖细胞衍生的VSMCs在动脉疾病中的证据和假定作用，这是决定祖细胞是否是血管疾病治疗靶点的必要前提。(C)2010年爱思唯尔公司All rights reserved.
Accumulation of vascular smooth muscle cells (VSMCs) in the tunica intima plays a major role in the pathogenesis of atherosclerosis and restenosis following endovascular procedures. Arterial VSMCs are heterogeneous even in the normal vessel wall and display different phenotypes in physiological and pathological conditions. In the classical paradigm, vascular wall injury induces VSMC de-differentiation, proliferation and migration from the media into the intima in response to growth factors and proteolytic agents. Accordingly, VSMCs in atherosclerotic plaques and in restenosis display a de-differentiated or 'synthetic' phenotype compared to a 'contractile' phenotype in the normal media. In contrast, recent studies have identified bone marrow and peripheral blood-derived endothelial and VSMC progenitors that may contribute to intimal formation in atherosclerosis, after arterial injury and in transplant atherosclerosis. The precise frequency of these bone marrow-derived vascular precursor cells is controversial and their role is unknown. In addition, additional data support the presence of a resident progenitor cell subpopulation and its involvement in the response of the adult arterial wall to damage or ischemia. This review will examine the evidence for and the putative role of progenitor cell-derived VSMCs in arterial disease, a necessary prerequisite before deciding whether progenitor cells are therapeutic targets in vascular disease. (C) 2010 Elsevier Inc. All rights reserved.