Molecular regulators and cell interactions make the blood-brain barrier a dynamic, highly selective interface crucial for CNS health and disease.
- 5 cites
Barrier Structure and Function Studies
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Restoring gut barrier function with targeted therapies could transform treatment of gut-brain interaction disorders, reducing symptoms in conditions like IBS and dyspepsia.
Up-regulation of CLDN2 during pancreatitis enhances ductal fluid transport and reduces disease severity, with knockout mice experiencing more severe pancreatitis.
- Open access
Cochlin, an extracellular matrix protein, enhances brain immune defense by reducing bacterial load, with levels increasing during infection in zebrafish, mice, and humans.
- Open access
Elevated blood-brain barrier permeability in sickle cell disease correlates with microstructural brain injury, with 79 plasma proteins linked to systemic pathways influencing BBB disruption.
Trogocytosis-related CLDN18.2 impairs CD8(+) T cell cytotoxicity and promotes pancreatic cancer progression by degrading β-catenin and inducing immune senescence.
- 2 cites
PAK4 is essential for vertex remodeling, maintaining epithelial integrity and barrier function, with its inhibition increasing vertices by 50% and causing junctional defects.
- Open access
- 1 cites
Molecular regulators and cell interactions make the blood-brain barrier a dynamic, highly selective interface crucial for CNS health and disease.
- 5 cites
Targeting claudins offers a promising new approach, with zolbetuximab becoming the first FDA-approved CLDN-18.2-targeted antibody for gastric cancer treatment.
TLR4 signaling in non-myeloid cells causes inflammation, Claudin-5 internalization, and vascular barrier breakdown in neonatal E. coli meningitis.
- Open access
Brain capillary endothelial cells autonomously repair injury through VEGFR2-dependent membrane extension, restoring blood flow within 24-48 hours in mice.
- Open access
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