Vascular smooth muscle stiffness and its role in aging

Andreea Trache, Michael P. Massett, Christopher R. Woodman

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

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.

Original languageEnglish
Title of host publicationMembrane Biomechanics
EditorsIrena Levitan, Andreea Trache, Andreea Trache
PublisherAcademic Press Inc.
Pages217-253
Number of pages37
ISBN (Print)9780128210215
DOIs
StatePublished - Jan 2020

Publication series

NameCurrent Topics in Membranes
Volume86
ISSN (Print)1063-5823

Keywords

  • Aging
  • Aorta
  • Cell adhesion
  • Cytoskeleton
  • Exercise
  • Mechanical signaling
  • Resistance arteries
  • Stiffness
  • Vascular smooth muscle cells
  • Vasoconstriction

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