Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action

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...

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Main Authors: Yi Zhu, Jing Qu, Li He, Feng Zhang, Zijing Zhou, Shanzhong Yang, Yong Zhou
Format: Article
Language:English
Published: Frontiers Media S.A. 2019-08-01
Series:Frontiers in Physiology
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fphys.2019.00852/full
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author Yi Zhu
Yi Zhu
Jing Qu
Jing Qu
Li He
Feng Zhang
Feng Zhang
Zijing Zhou
Zijing Zhou
Shanzhong Yang
Yong Zhou
author_facet Yi Zhu
Yi Zhu
Jing Qu
Jing Qu
Li He
Feng Zhang
Feng Zhang
Zijing Zhou
Zijing Zhou
Shanzhong Yang
Yong Zhou
author_sort Yi Zhu
collection DOAJ
description 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 Ca2+ 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 Ca2+-dependent regulation of VSMC stiffness and adhesion to the ECM, providing novel insights into the mechanism of calcium action.
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spelling doaj.art-cb1fefcd14ff43869a79d053ad8f42bd2022-12-22T03:45:08ZengFrontiers Media S.A.Frontiers in Physiology1664-042X2019-08-011010.3389/fphys.2019.00852458924Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of ActionYi Zhu0Yi Zhu1Jing Qu2Jing Qu3Li He4Feng Zhang5Feng Zhang6Zijing Zhou7Zijing Zhou8Shanzhong Yang9Yong Zhou10Division of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama-Birmingham, Birmingham, AL, United StatesDalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, MO, United StatesDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama-Birmingham, Birmingham, AL, United StatesDepartment of Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama-Birmingham, Birmingham, AL, United StatesDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama-Birmingham, Birmingham, AL, United StatesDepartment of Ophthalmology, The Second Xiangya Hospital, Central-South University, Changsha, ChinaDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama-Birmingham, Birmingham, AL, United StatesDepartment of Respiratory Medicine, The Second Xiangya Hospital, Central-South University, Changsha, ChinaDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama-Birmingham, Birmingham, AL, United StatesDivision of Pulmonary, Allergy and Critical Care Medicine, Department of Medicine, University of Alabama-Birmingham, Birmingham, AL, United StatesVascular 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 Ca2+ 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 Ca2+-dependent regulation of VSMC stiffness and adhesion to the ECM, providing novel insights into the mechanism of calcium action.https://www.frontiersin.org/article/10.3389/fphys.2019.00852/fullvascular smooth muscle cellcalciumelasticityadhesionextracellular matrix-integrin-cytoskeletal axis
spellingShingle Yi Zhu
Yi Zhu
Jing Qu
Jing Qu
Li He
Feng Zhang
Feng Zhang
Zijing Zhou
Zijing Zhou
Shanzhong Yang
Yong Zhou
Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action
Frontiers in Physiology
vascular smooth muscle cell
calcium
elasticity
adhesion
extracellular matrix-integrin-cytoskeletal axis
title Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action
title_full Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action
title_fullStr Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action
title_full_unstemmed Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action
title_short Calcium in Vascular Smooth Muscle Cell Elasticity and Adhesion: Novel Insights Into the Mechanism of Action
title_sort calcium in vascular smooth muscle cell elasticity and adhesion novel insights into the mechanism of action
topic vascular smooth muscle cell
calcium
elasticity
adhesion
extracellular matrix-integrin-cytoskeletal axis
url https://www.frontiersin.org/article/10.3389/fphys.2019.00852/full
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