Department of Biomedicine, Laboratory for Signal Transduction, University Hospital Basel and University of Basel, Basel, Switzerland.
Department of Biomedicine, Laboratory for Signal Transduction, University Hospital Basel and University of Basel, Basel, Switzerland.
Cell Signal. 2018 May;45:23-42. doi: 10.1016/j.cellsig.2018.01.023. Epub 2018 Feb 3.
Vascular smooth muscle cells (SMCs) phenotypes span a reversible continuum from quiescent/contractile (differentiated) to proliferative/synthetic (dedifferentiated) enabling them to perform a diversity of functions that are context-dependent and important for vascular tone-diameter homeostasis, vasculogenesis, angiogenesis or vessel reparation after injury. Dysregulated phenotype modulation and failure to maintain/regain the mature differentiated and contractile phenotypic state is pivotal in the development of vascular diseases such as atherosclerosis and restenosis after angioplasty and coronary bypass grafting. Many functions of SMCs such as adhesion, migration, proliferation, contraction, differentiation and apoptosis are regulated by a broad spectrum of cell-cell and cell-matrix adhesion molecules. Cadherins represent a superfamily of cell surface homophilic adhesion molecules with fundamental roles in morphogenetic and differentiation processes during development and in the maintenance of tissue integrity and homeostasis in adults. The cadherins have major inputs on signalling pathways and cytoskeletal assemblies that participate in regulating processes such as cell polarity, migration, proliferation, survival, phenotype and differentiation. Abnormalities in these processes have long been recognized to underlie pathological SMC-driven reparation, but knowledge on the involvement of cadherins is remarkably limited. This article presents a comprehensive review of cadherin family members currently identified on vascular SMCs in relation to their functions, molecular mechanisms of action and relevance for vascular pathology.
血管平滑肌细胞（SMC）表型跨越一个可逆的连续体，从静止/收缩（分化）到增殖/合成（去分化），使它们能够执行多种功能，这些功能是上下文相关的，对血管张力-直径平衡、血管发生、血管生成或损伤后血管修复很重要。表型调节失调和未能维持/恢复成熟分化和收缩表型状态是血管疾病（如动脉粥样硬化和血管成形术后再狭窄和冠状动脉旁路移植术）发展的关键。SMC 的许多功能，如粘附、迁移、增殖、收缩、分化和凋亡，都受到广泛的细胞间和细胞基质粘附分子的调节。钙黏蛋白是细胞表面同源性粘附分子的超家族，在发育过程中的形态发生和分化过程以及在成人组织完整性和内稳态的维持中发挥着重要作用。钙黏蛋白对参与调节细胞极性、迁移、增殖、存活、表型和分化等过程的信号通路和细胞骨架组装有重要影响。这些过程中的异常早已被认为是病理性 SMC 驱动修复的基础，但对钙黏蛋白的参与知之甚少。本文全面回顾了目前在血管 SMC 中鉴定的钙黏蛋白家族成员，以及它们的功能、作用的分子机制及其与血管病理学的相关性。
