Vascular smooth muscle cells (VSMCs) are the predominant cell type in the arterial wall and normally adopt a quiescent, contractile phenotype to regulate vascular tone. In the arterial wall, VSMCs are exposed to multiple mechanical cues, including stretch and matrix stiffness, which regulate VSMC contraction. However, during ageing and in vascular disease, such as atherosclerosis, hypertension and vascular calcification, the arterial wall stiffens and VSMC contraction contributes to this process. VSMCs display remarkable plasticity and changes in their mechanical environment promote VSMCs to adopt a proliferative, synthetic phenotype. VSMC phenotypic modulation is associated with altered expression of contractile proteins that generate actomyosin-based force. However, our understanding of precise mechanisms whereby altered mechanical landscape and mechanotransduction influence VSMC contraction remains limited. In this review, we discuss the present literature describing how VSMCs sense and respond to changes in their mechanical environment and how these changes influence VSMC contraction.
- Matrix stiffness
- vascular smooth muscle cell