Mechanical stretch modulates cellular functions in vascular smooth muscle cells, endothelial cells, and cardiac myocytes, playing a vital role in cardiovascular disease pathogenesis.
Understanding the molecular mechanisms of mechanical stretch on cardiovascular cells provides insights into the pathogenesis and potential therapies for cardiovascular diseases.
Cells in the cardiovascular system are permanently subjected to mechanical forces due to the pulsatile nature of blood flow and shear stress, created by the beating heart. These haemodynamic forces play an important role in the regulation of vascular development, remodelling, wound healing and atherosclerotic lesion formation. Mechanical stretch can modulate several different cellular functions in VSMCs (vascular smooth muscle cells). These functions include, but are not limited to, cell alignment and differentiation, migration, survival or apoptosis, vascular remodelling, and autocrine and paracrine functions. Laminar shear stress exerts anti-apoptotic, anti-atherosclerotic and antithrombotic effects on ECs (endothelial cells). Mechanical stretch of cardiac myocytes can modulate growth, apoptosis, electric remodelling, alterations in gene expression, and autocrine and paracrine effects. The aim of the present review is primarily to summarize the cellular and molecular effects of mechanical stretch on vascular cells and cardiac myocytes, emphasizing the molecular mechanisms underlying the regulation. Knowledge of the impact of mechanical stretch on the cardiovascular system is vital to the understanding of the pathogenesis of cardiovascular diseases, and is also crucial to provide new insights into the prevention and therapy of cardiovascular diseases.
Kou‐Gi Shyu (Mon,) conducted a review in Cardiovascular diseases. Mechanical stretch was evaluated. Mechanical stretch modulates cellular functions in vascular smooth muscle cells, endothelial cells, and cardiac myocytes, playing a vital role in cardiovascular disease pathogenesis.