Biomechanical signal communication in vascular smooth muscle cells

Biomechanical stresses are closely associated with cardiovascular development and diseases. In vivo, vascular smooth muscle cells are constantly stimulated by biomechanical factors caused by increased blood pressure leading to the non-specific activation of cell transmembrane proteins. Thus, various intracellular signal molecules are simultaneously activated via signaling cascades, which are closely related to alterations in the differentiation, phenotype, inflammation, migration, pyroptosis, calcification, proliferation, and apoptosis of vascular smooth muscle cells. Meanwhile, mechanical stress-induced miRNAs and epigenetics modification on vascular smooth muscle cells play critical roles as well. Eventually, the overall pathophysiology of the cells is altered, resulting in the development of many major clinical diseases, including hypertension, atherosclerosis, grafted venous atherosclerosis, and aneurysm, among others. In this paper, important advances in mechanical signal communication in vascular smooth muscle cells are reviewed.