Abstract
AbstractThe stiffness of arterial wall in response to cardiovascular diseases has been associated with the changes in extracellular matrix (ECM) proteins,i.e., collagen and elastin. Vascular smooth muscle cells (VSMCs) helped to regulate the ECM reorganizations and thus contributed to arterial stiffness. This article reviewed experimental and computational studies for quantifying the roles of ECM proteins and VSMCs in mechanical properties of arteries, including nanostructure and mechanical properties of VSMCs and ECMs, cell-ECM interaction, and biomimetic gels/scaffolds induced contractile properties and phenotype changing of VSMCs. This work will facilitate our understanding of how the microenvironments and mechanotransduction impact and regulate the arterial adaptation.
Highlights
The stiffness of arterial wall in response to cardiovascular diseases has been associated with the changes in extracellular matrix (ECM) proteins, i.e., collagen and elastin
This article reviewed experimental and computational studies for quantifying the roles of ECM proteins and Vascular smooth muscle cells (VSMCs) in mechanical properties of arteries, including nanostructure and mechanical properties of VSMCs and ECMs, cell-ECM interaction, and biomimetic gels/scaffolds induced contractile properties and phenotype changing of VSMCs
Advanced glycation end-products (AGEs), which accumulate slowly with normal aging or in diabetes at a faster rate, has been considered as a major index factor for arterial wall stiffening [82, 83]. This was attributed to the increased protein– protein crosslinks on the collagen molecule [84, 85] and implied that collagen/elastin components alone are not the only inclusive parts to determine the arterial stiffness in certain situations
Summary
The cytoskeletal of vascular smooth muscles encompasses filaments and organelles. The density and number of these components can vary with respect to different internal and external signals [1, 2]. These filaments play a principal role in the mechanical properties of vascular smooth muscle cells including proliferation [3], differentiation [4, 5], cell migration [6], and apoptosis [7, 8]. Artery and its cellular components are continuously exposed to hemodynamic stimuli including cyclic strain, flow shear stress, and blood pressure [46, 47] These mechanical loadings correlated with VSMC behaviors, ECM remodeling, and vasoregulation [48]. Considering the limitation in reproducing a complex in vivo ECM environment, the load sharing of VSMCs with respect to these structural components of ECM remained to be explored
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