TARGETING VASCULAR SMOOTH MUSCLE CELL TO IMPROVE ARTERIAL STIFFNESS

DOI

10.1016/j.artres.2017.10.008How to use a DOI?

Abstract

Hypertension and arterial aging engage a plethora of key signaling pathways that act in concert to induce vascular smooth muscle cell (VSMC) phenotypic changes leading to vascular degeneration and extracellular matrix (ECM) changes responsible for alterations of the mechanical properties of the vascular wall. This review highlights proof-of-concept examples of components of the extracellular matrix, VSMC receptors which connect extracellular and intracellular structures and signaling pathways regulating changes in mechanotransduction and vascular homeostasis. This presentation presents new directions in the role of vascular smooth muscle cells VSMCs traditionally limited to regulation of contractile properties and synthesis of ECM proteins. VSMCs may exert negative feedback or positive feedback on ECM stiffness and mechanical load via stabilized focal adhesions, activated Rho-ROCK signaling pathways or actomyosin contraction. Understanding the mechanisms of cellular stiffness are also important to appreciate its contribution to mechanical properties at the tissue-level. Many other cell types, including macrophages, could participate to inflammation and VSMC stiffness leading to fibrosis of the arterial wall. In view of the multitude roles of VSMCs and feedback controls, only omic approaches and computational models may extrapolate the overall effects on the vascular wall in light of hemodynamics and complex interactions amongst differentially sized vessels. The use of novel animal models with multiple genetic manipulations of VSMC signaling pathways can provide further insight into the link between large vessel stiffness and small vessel dysfunction.

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TY  - JOUR
AU  - Patrick Lacolley
PY  - 2017
DA  - 2017/12/06
TI  - TARGETING VASCULAR SMOOTH MUSCLE CELL TO IMPROVE ARTERIAL STIFFNESS
JO  - Artery Research
SP  - 45
EP  - 45
VL  - 20
IS  - C
SN  - 1876-4401
UR  - https://doi.org/10.1016/j.artres.2017.10.008
DO  - 10.1016/j.artres.2017.10.008
ID  - Lacolley2017
ER  -