Endothelial Barrier Dynamics in Acute Lung Injury
Summary
The pulmonary microvascular endothelium forms a semipermeable barrier that regulates fluid and solute exchange between the blood and the alveolar interstitium. In acute lung injury (ALI), a combination of inflammatory mediators, mechanical stress and endothelial cell dysfunction leads to disruption of intercellular junctions and cytoskeletal remodelling, resulting in increased vascular permeability and pulmonary oedema. Central to this process are adherens and tight junction proteins, the Rho family of small GTPases and their downstream kinases, which together coordinate contractile forces and junctional integrity. Dysregulated signalling via pathways such as RhoA–ROCK, Rac1–LIMK1 and NF-κB drives cytoskeletal contraction, junctional disassembly and leukocyte extravasation. Restoring barrier function through modulation of growth factor receptors, inhibition of contractile kinases or enhancement of junctional stabilisers represents a promising therapeutic strategy. Advances in our understanding of endothelial barrier dynamics are critical to developing treatments that limit vascular leak and improve outcomes in patients with ALI and acute respiratory distress syndrome.
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Endothelial Barrier Dynamics in Acute Lung Injury publication trend
The graph below shows the total number of articles in endothelial barrier dynamics in acute lung injury across all publications each year (not limited to Nature Index journals).
Technical terms
Endothelial barrier: Layer of interconnected endothelial cells that controls fluid, solute and cell traffic between blood and tissue.
Adherens junctions: Cell–cell adhesion complexes, chiefly composed of VE-cadherin, that maintain vascular cohesion and restrict paracellular permeability.
Rho-associated coiled-coil-forming protein kinase (ROCK): Effector kinase downstream of RhoA that drives actomyosin contraction and junctional tension.
Rac1: Small GTPase that promotes actin polymerisation and lamellipodial dynamics to stabilise cell–cell contacts.
Fibroblast growth factor receptor 1 (FGFR1): Receptor tyrosine kinase essential for endothelial cell survival, proliferation and barrier maintenance.
References
- Deficiency of endothelial FGFR1 signaling via upregulation of ROCK2 activity aggravated ALI/ARDS. Frontiers in Immunology (2023).
- Tetramethylpyrazine ameliorates acute lung injury by regulating the Rac1/LIMK1 signaling pathway. Frontiers in Pharmacology (2023).
- Fibroblast growth factor-2 alleviates the capillary leakage and inflammation in sepsis. Molecular Medicine (2020).
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