Zhu Yi, Qu Jing, He Li, Zhang Feng, Zhou Zijing, Yang Shanzhong, Zhou Yong
Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama-Birmingham, Birmingham, AL, United States.
Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, MO, United States.
Front Physiol. 2019 Aug 7;10:852. doi: 10.3389/fphys.2019.00852. eCollection 2019.
Vascular smooth muscle cells (VSMCs) are the predominant cell type in the arterial wall. These cells play a critical role in maintaining vascular homeostasis including vasoconstriction and vasodilatation through active contraction and relaxation. Dysregulation of VSMC function alters the response of blood vessels to mechanical stress, contributing to the pathogenesis of vascular diseases, particularly atherosclerosis and hypertension. The stiffness of VSMCs is a major regulator of vascular function. Previous studies suggest that intracellular Ca controls the stiffness of VSMCs by a mechanism involving myosin contractile apparatus. More recent studies highlight important functions of cytoskeletal α-smooth muscle actin (α-SMA), α5β1 integrin, and integrin-mediated cell-extracellular matrix (ECM) interactions in Ca-dependent regulation of VSMC stiffness and adhesion to the ECM, providing novel insights into the mechanism of calcium action.
血管平滑肌细胞（VSMC）是动脉壁中的主要细胞类型。这些细胞在维持血管稳态中起关键作用，包括通过主动收缩和舒张实现血管收缩和舒张。VSMC功能失调会改变血管对机械应力的反应，导致血管疾病，特别是动脉粥样硬化和高血压的发病机制。VSMC的硬度是血管功能的主要调节因子。先前的研究表明，细胞内钙通过涉及肌球蛋白收缩装置的机制控制VSMC的硬度。最近的研究强调了细胞骨架α-平滑肌肌动蛋白（α-SMA）、α5β1整合素以及整合素介导的细胞-细胞外基质（ECM）相互作用在钙依赖性调节VSMC硬度和与ECM粘附方面的重要功能，为钙作用机制提供了新的见解。
