当前位置: X-MOL 学术Cell. Signal. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Cadherins in vascular smooth muscle cell (patho)biology: Quid nos scimus?
Cellular Signalling ( IF 4.8 ) Pub Date : 2018-02-03 , DOI: 10.1016/j.cellsig.2018.01.023
Agne Frismantiene , Maria Philippova , Paul Erne , Therese J. Resink

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.



中文翻译:

钙黏着蛋白在血管平滑肌细胞(病理)生物学中的作用:难道不是坐骨神经痛吗?

血管平滑肌细胞(SMCs)表型涵盖了从静止/收缩(分化)到增生/合成(去分化)的可逆连续体,使它们能够执行多种功能,这些功能取决于上下文,并且对于血管直径直径的稳态,脉管生成,损伤后的血管生成或血管修复。在血管成形术和冠状动脉搭桥术后,动脉粥样硬化和再狭窄等血管疾病的发展至关重要。SMC的许多功能,例如粘附,迁移,增殖,收缩,分化和凋亡均受广泛的细胞-细胞和细胞-基质粘附分子的调节。钙黏着蛋白代表细胞表面同源粘附分子的超家族,其在发育过程中的形态发生和分化过程以及维持成人的组织完整性和体内平衡方面具有基本作用。钙黏着蛋白主要参与信号传导途径和细胞骨架组装,这些细胞参与调节过程,例如细胞极性,迁移,增殖,存活,表型和分化。长期以来,人们已认识到这些过程的异常是病理性SMC驱动的修复的基础,但有关钙粘蛋白参与的知识却非常有限。本文对目前在血管平滑肌细胞上鉴定的钙粘着蛋白家族成员的功能,作用的分子机制以及与血管病理学的相关性进行了全面的综述。

更新日期:2018-02-03
down
wechat
bug