Endothelial Plasticity: Shifting Phenotypes through Force Feedback

Area of Science:

• Vascular biology
• Cellular plasticity
• Pathophysiology

Background:

• Endothelial cells face diverse biochemical and hemodynamic stimuli.
• Endothelial cells exhibit plasticity, crucial for adaptation and organ-specific function.
• Proatherogenic stimuli can induce maladaptive endothelial plasticity, contributing to disease.

Purpose of the Study:

• To explore how shear stress and cyclic strain modulate Endothelial-to-Mesenchymal Transition (EndMT).
• To discuss the role of EndMT in the pathogenesis of atherosclerosis and pulmonary arterial hypertension.

Main Methods:

• Review of existing literature on endothelial cell plasticity and EndMT.
• Analysis of the impact of hemodynamic forces on endothelial phenotype.
• Discussion of disease mechanisms involving EndMT.

Main Results:

• Shear stress and cyclic strain are significant modulators of endothelial cell phenotype and function.
• EndMT, once thought confined to development, is now recognized as a pathological process in various diseases.
• Adverse endothelial plasticity, including EndMT, is implicated in atherosclerosis and pulmonary arterial hypertension.

Conclusions:

• Hemodynamic forces play a critical role in regulating endothelial plasticity and EndMT.
• Understanding EndMT modulation by mechanical forces is key to developing therapies for vascular diseases.
• EndMT represents a crucial link between mechanical stimuli and the development of atherosclerosis and pulmonary arterial hypertension.