Vascular smooth muscle stiffness and its role in aging
Vascular smooth muscle cells (VSMC) are now considered important contributors to the pathophysiological and biophysical mechanisms underlying arterial stiffening in aging. Here, we review mechanisms whereby VSMC stiffening alters vascular function and contributes to the changes in vascular stiffenin...
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Published in | Current topics in membranes Vol. 86; pp. 217 - 253 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
United States
2020
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Subjects | |
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Abstract | Vascular smooth muscle cells (VSMC) are now considered important contributors to the pathophysiological and biophysical mechanisms underlying arterial stiffening in aging. Here, we review mechanisms whereby VSMC stiffening alters vascular function and contributes to the changes in vascular stiffening observed in aging and cardiovascular disease. Vascular stiffening in arterial aging was historically associated with changes in the extracellular matrix; however, new evidence suggests that endothelial and vascular smooth muscle cell stiffness also contribute to overall blood vessel stiffness. Furthermore, VSMC play an integral role in regulating matrix deposition and vessel wall contractility via interaction between the actomyosin contractile unit and adhesion structures that anchor the cell within the extracellular matrix. Aged-induce phenotypic modulation of VSMC from a contractile to a synthetic phenotype is associated with decreased cellular contractility and increased cell stiffness. Aged VSMC also display reduced mechanosensitivity and adaptation to mechanical signals from their microenvironment due to impaired intracellular signaling. Finally, evidence for decreased contractility in arteries from aged animals demonstrate that changes at the cellular level result in decreased functional properties at the tissue level. |
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AbstractList | Vascular smooth muscle cells (VSMC) are now considered important contributors to the pathophysiological and biophysical mechanisms underlying arterial stiffening in aging. Here, we review mechanisms whereby VSMC stiffening alters vascular function and contributes to the changes in vascular stiffening observed in aging and cardiovascular disease. Vascular stiffening in arterial aging was historically associated with changes in the extracellular matrix; however, new evidence suggests that endothelial and vascular smooth muscle cell stiffness also contribute to overall blood vessel stiffness. Furthermore, VSMC play an integral role in regulating matrix deposition and vessel wall contractility via interaction between the actomyosin contractile unit and adhesion structures that anchor the cell within the extracellular matrix. Aged-induce phenotypic modulation of VSMC from a contractile to a synthetic phenotype is associated with decreased cellular contractility and increased cell stiffness. Aged VSMC also display reduced mechanosensitivity and adaptation to mechanical signals from their microenvironment due to impaired intracellular signaling. Finally, evidence for decreased contractility in arteries from aged animals demonstrate that changes at the cellular level result in decreased functional properties at the tissue level. |
Author | Woodman, Christopher R Massett, Michael P Trache, Andreea |
Author_xml | – sequence: 1 givenname: Andreea surname: Trache fullname: Trache, Andreea email: trache@tamu.edu organization: Department of Medical Physiology, Texas A&M University Health Science Center, Bryan, TX, United States; Department of Biomedical Engineering, Texas A&M University, College Station, TX, United States. Electronic address: trache@tamu.edu – sequence: 2 givenname: Michael P surname: Massett fullname: Massett, Michael P organization: Department of Kinesiology and Sport Management, Texas Tech University, Lubbock, TX, United States – sequence: 3 givenname: Christopher R surname: Woodman fullname: Woodman, Christopher R organization: Department of Health and Kinesiology, Texas A&M University, College Station, TX, United States |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33837694$$D View this record in MEDLINE/PubMed |
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Keywords | Exercise Cell adhesion Vasoconstriction Aging Resistance arteries Aorta Cytoskeleton Stiffness Mechanical signaling Vascular smooth muscle cells |
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