Origin and differentiation of vascular smooth muscle cells.
Origin and differentiation of vascular smooth muscle cells.
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DOI：
10.1113/jp270033
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发表时间：
2015-07-15
期刊：
影响因子：
--
通讯作者：
Xu Q
中科院分区：
文献类型：
--
作者：
Wang G;Jacquet L;Karamariti E;Xu Q
血管平滑肌细胞（Vascular smooth muscle cell，SMC）是血管壁的主要结构成分，在维持血管结构和功能方面起着重要作用。在胚胎发生过程中，SMC从其祖细胞的募集是胚胎血管系统形成的重要步骤。动脉壁中的SMC大多数是静止的，但在成人中可以显示收缩表型。在病理生理条件下，即内皮功能障碍或损伤后的血管重塑，中膜中发现的收缩性SMC转变为分泌型，这将促进它们迁移到内膜并增殖以促成新生内膜病变的能力。然而，最近的证据表明，在血管重塑（如新生内膜增生和动脉硬化）过程中，血管壁中存在的大量干/祖细胞的动员和募集在很大程度上是内膜中SMC积聚的原因。因此，了解控制SMC从血管祖细胞分化的调控机制对于探索潜在临床应用的治疗靶点至关重要。在这篇文章中，我们审查的起源和分化的SMCs从干/祖细胞在心血管发育和成人，突出的环境线索和信号通路，控制表型调制血管系统内。
Vascular smooth muscle cells (SMCs), a major structural component of the vessel wall, not only play a key role in maintaining vascular structure but also perform various functions. During embryogenesis, SMC recruitment from their progenitors is an important step in the formation of the embryonic vascular system. SMCs in the arterial wall are mostly quiescent but can display a contractile phenotype in adults. Under pathophysiological conditions, i.e. vascular remodelling after endothelial dysfunction or damage, contractile SMCs found in the media switch to a secretory type, which will facilitate their ability to migrate to the intima and proliferate to contribute to neointimal lesions. However, recent evidence suggests that the mobilization and recruitment of abundant stem/progenitor cells present in the vessel wall are largely responsible for SMC accumulation in the intima during vascular remodelling such as neointimal hyperplasia and arteriosclerosis. Therefore, understanding the regulatory mechanisms that control SMC differentiation from vascular progenitors is essential for exploring therapeutic targets for potential clinical applications. In this article, we review the origin and differentiation of SMCs from stem/progenitor cells during cardiovascular development and in the adult, highlighting the environmental cues and signalling pathways that control phenotypic modulation within the vasculature.