Vascular mechanical forces and vascular diseases

Background

Blood vessels are continuously exposed to mechanical forces, mainly including shear stress, cyclic stretch, and hydrostatic pressure. These forces regulate the functions of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) through complex mechanosensing and signal transduction pathways, which are essential for maintaining vascular homeostasis. However, under pathological conditions, they can contribute to the development of vascular diseases, such as atherosclerosis, hypertension, and aortic aneurysm.

Aim of review

This review aims to synthesize the mechanosensors and downstream signaling pathways of vascular mechanical forces in ECs and VSMCs, emphasizing their effects on cell behaviors and their involvement in the onset and progression of atherosclerosis, hypertension and aortic aneurysms.

Key scientific concepts of review

Multiple molecules and structures – including ion channels, G-protein coupled receptors, cellular junction molecules, and other membrane structures – act as mechanosensors of vascular mechanical forces and trigger multiple downstream signal transduction pathways. The pathological alterations in shear stress, cyclic stretch, and hydrostatic pressure regulate the functions and behaviors of ECs and VSMCs, including cellular proliferation, migration, apoptosis, oxidative stress, endothelial permeability, etc. These responses induce vascular inflammation, dysfunction and remodeling, which eventually contributes to the onset and progression of atherosclerosis, hypertension, and aortic aneurysms. This review also highlights the underestimated role of hydrostatic pressure in atherosclerosis and hypertension, as well as other research gaps and future directions for vascular mechanical forces research. Understanding and therapeutically modulating these biomechanical pathways may ultimately facilitate more effective prevention and treatment of vascular diseases