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Vascular smooth muscle cells and arterial stiffening : relevance in development, aging, and disease

(2017) PHYSIOLOGICAL REVIEWS. 97(4). p.1555-1617
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Abstract
The cushioning function of large arteries encompasses distension during systole and recoil during diastole which transforms pulsatile flow into a steady flow in the microcirculation. Arterial stiffness, the inverse of distensibility, has been implicated in various etiologies of chronic common and monogenic cardiovascular diseases and is a major cause of morbidity and mortality globally. The first components that contribute to arterial stiffening are extracellular matrix (ECM) proteins that support the mechanical load, while the second important components are vascular smooth muscle cells (VSMCs), which not only regulate actomyosin interactions for contraction but mediate also mechanotransduction in cell-ECM homeostasis. Eventually, VSMC plasticity and signaling in both conductance and resistance arteries are highly relevant to the physiology of normal and early vascular aging. This review summarizes current concepts of central pressure and tensile pulsatile circumferential stress as key mechanical determinants of arterial wall remodeling, cell-ECM interactions depending mainly on the architecture of cytoskeletal proteins and focal adhesion, the large/small arteries cross-talk that gives rise to target organ damage, and inflammatory pathways leading to calcification or atherosclerosis. We further speculate on the contribution of cellular stiffness along the arterial tree to vascular wall stiffness. In addition, this review provides the latest advances in the identification of gene variants affecting arterial stiffening. Now that important hemodynamic and molecular mechanisms of arterial stiffness have been elucidated, and the complex interplay between ECM, cells, and sensors identified, further research should study their potential to halt or to reverse the development of arterial stiffness.
Keywords
PULSE-WAVE VELOCITY, EHLERS-DANLOS-SYNDROME, CONVERTING-ENZYME-INHIBITION, INTIMA-MEDIA THICKNESS, SPONTANEOUSLY, HYPERTENSIVE-RATS, WILLIAMS-BEUREN-SYNDROME, CHRONIC KIDNEY-DISEASE, GROWTH-FACTOR-BETA, CARDIOVAGAL BAROREFLEX SENSITIVITY, ISOLATED, SYSTOLIC HYPERTENSION

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Citation

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Chicago
Lacolley, Patrick, Véronique Regnault, Patrick Segers, and Stéphane Laurent. 2017. “Vascular Smooth Muscle Cells and Arterial Stiffening : Relevance in Development, Aging, and Disease.” Physiological Reviews 97 (4): 1555–1617.
APA
Lacolley, P., Regnault, V., Segers, P., & Laurent, S. (2017). Vascular smooth muscle cells and arterial stiffening : relevance in development, aging, and disease. PHYSIOLOGICAL REVIEWS, 97(4), 1555–1617.
Vancouver
1.
Lacolley P, Regnault V, Segers P, Laurent S. Vascular smooth muscle cells and arterial stiffening : relevance in development, aging, and disease. PHYSIOLOGICAL REVIEWS. 2017;97(4):1555–617.
MLA
Lacolley, Patrick et al. “Vascular Smooth Muscle Cells and Arterial Stiffening : Relevance in Development, Aging, and Disease.” PHYSIOLOGICAL REVIEWS 97.4 (2017): 1555–1617. Print.
@article{8556470,
  abstract     = {The cushioning function of large arteries encompasses distension during systole and recoil during diastole which transforms pulsatile flow into a steady flow in the microcirculation. Arterial stiffness, the inverse of distensibility, has been implicated in various etiologies of chronic common and monogenic cardiovascular diseases and is a major cause of morbidity and mortality globally. The first components that contribute to arterial stiffening are extracellular matrix (ECM) proteins that support the mechanical load, while the second important components are vascular smooth muscle cells (VSMCs), which not only regulate actomyosin interactions for contraction but mediate also mechanotransduction in cell-ECM homeostasis. Eventually, VSMC plasticity and signaling in both conductance and resistance arteries are highly relevant to the physiology of normal and early vascular aging. This review summarizes current concepts of central pressure and tensile pulsatile circumferential stress as key mechanical determinants of arterial wall remodeling, cell-ECM interactions depending mainly on the architecture of cytoskeletal proteins and focal adhesion, the large/small arteries cross-talk that gives rise to target organ damage, and inflammatory pathways leading to calcification or atherosclerosis. We further speculate on the contribution of cellular stiffness along the arterial tree to vascular wall stiffness. In addition, this review provides the latest advances in the identification of gene variants affecting arterial stiffening. Now that important hemodynamic and molecular mechanisms of arterial stiffness have been elucidated, and the complex interplay between ECM, cells, and sensors identified, further research should study their potential to halt or to reverse the development of arterial stiffness.},
  author       = {Lacolley, Patrick and Regnault, Véronique and Segers, Patrick and Laurent, Stéphane},
  issn         = {0031-9333},
  journal      = {PHYSIOLOGICAL REVIEWS},
  keywords     = {PULSE-WAVE VELOCITY,EHLERS-DANLOS-SYNDROME,CONVERTING-ENZYME-INHIBITION,INTIMA-MEDIA THICKNESS,SPONTANEOUSLY,HYPERTENSIVE-RATS,WILLIAMS-BEUREN-SYNDROME,CHRONIC KIDNEY-DISEASE,GROWTH-FACTOR-BETA,CARDIOVAGAL BAROREFLEX SENSITIVITY,ISOLATED,SYSTOLIC HYPERTENSION},
  language     = {eng},
  number       = {4},
  pages        = {1555--1617},
  title        = {Vascular smooth muscle cells and arterial stiffening : relevance in development, aging, and disease},
  url          = {http://dx.doi.org/10.1152/physrev.00003.2017},
  volume       = {97},
  year         = {2017},
}

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