Mechanotransduction in Endothelial Cell Function

Mechanotransduction is the process whereby endothelial cells perceive and respond to mechanical forces inherent to blood flow and pressure within the vasculature. Endothelial cells lining the inner surface of blood vessels convert fluid shear stress, cyclic stretch and hydrostatic pressure into intracellular biochemical signals. These signals regulate cell morphology, cytoskeletal remodelling and gene expression pivotal to vascular homeostasis, barrier function and inflammatory modulation. Under laminar shear stress, endothelial cells elongate and align in the direction of flow, forming specialised membrane domains enriched in mechanosensitive proteins and lipid microdomains. Activation of mechanosensitive ion channels and adaptor complexes leads to calcium influx, activation of endothelial nitric oxide synthase and downstream effectors that maintain vascular tone and suppress inflammatory gene expression. Dysregulation of mechanotransduction pathways contributes to vascular pathologies such as atherosclerosis, hypertension and arteriovenous malformations. Elucidating the molecular basis of force transduction in endothelial cells is therefore crucial for understanding vascular development, disease progression and the design of targeted therapeutics.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Mechanotransduction in Endothelial Cell Function publication trend

The graph below shows the total number of articles in mechanotransduction in endothelial cell function across all publications each year (not limited to Nature Index journals).

Technical terms

Mechanotransduction: The conversion of mechanical stimuli such as shear stress or stretch into intracellular biochemical signals by cells.

Shear stress: The tangential force per unit area exerted by fluid flow on the endothelial surface, critical for vascular function.

Caveolin-1-rich microdomain: Specialised, cholesterol-rich regions of the plasma membrane that organise signalling proteins and lipids.

Transient receptor potential vanilloid 4 (TRPV4) channel: A mechanosensitive ion channel that mediates calcium influx in response to physical forces.

Endothelial nitric oxide synthase (eNOS): An enzyme that produces nitric oxide, a vasodilator and anti-inflammatory mediator.

References

1. Mechanosensitive membrane domains regulate calcium entry in arterial endothelial cells to protect against inflammation. Journal of Clinical Investigation (2024).
2. A 96-wells fluidic system for high-throughput screenings under laminar high wall shear stress conditions. Microsystems & Nanoengineering (2023).