A specific SARS-CoV-2 proteins that affect the vascular permeability and impairs the functionality of other significant organs has been identified.

Pathological vessel leakage in mouse retinopathy models depends on VE-cadherin Y685 phosphorylation status, which in turn is regulated by a signaling cascade originating with VEGFR2 Y949 phosphorylation.

Arpin regulates actomyosin contractility and endothelial barrier integrity by controlling the activity of the kinases ROCK1 and ZIPK, but not Arp2/3.

Matrix metalloprotease (MMP)-14 cleaves Tie2 at three distinct sites within the fibronectin type-III (FN3) domain and its pharmacological blockade inhibits Tie2 pathological shedding to exert barrier protective effects.

Elevating beta-catenin signaling converts endothelial cells in typically fenestrated central nervous system vasculature to a blood-brain barrier (BBB) phenotype and promotes a BBB gene expression program and chromatin landscape.

Proteins produced by mast cells modulate the permeability of blood vessels, and may determine whether patients infected with dengue virus develop life-threatening complications.

Direct reprogramming of smooth muscle cells from HGPS patients revealed that BMP4 is a key contributor of vascular degeneration and might represent a new therapeutic target.

Normal hematopoietic stem and progenitor cells slow the regeneration of their niche after injury to minimize leakage from the niche vasculature.

Organ and vessel-type-specific differences in endothelial cell barrier composition and properties uncover the distinct importance of the major tight junction protein Claudin5 in restricting agonist-induced leakage.