Claudin-5 (CLDN5)

Claudin-5 is a barrier-forming tight junction protein of the claudin family, encoded by the CLDN5 gene[1][3]. It plays a central role in endothelial cell tight junctions—especially in the blood-brain barrier—by controlling paracellular permeability and limiting diffusion of ions and small molecules between cells[1][2][3][4][5]. Its expression and localization are tightly regulated by other junctional proteins and supporting cells (pericytes, astrocytes), and mutations or dysregulation lead to increased barrier permeability, which can contribute to neuropsychiatric and neurological disorders[3]. Claudin-5’s molecular interactions include binding with other claudins and partnering with scaffolding proteins such as ZO-1 to form and maintain tight junctions[1][5]. Its importance in endothelium is highlighted by research in animal models; for example, mice lacking claudin-5 show lethal blood-brain barrier failure soon after birth[3]. Finally, claudin-5 has been associated with human diseases such as velocardiofacial syndrome due to mutations, and is under investigation as both a disease biomarker and a potential therapeutic target for modulating vascular permeability[3][5].

Other names

Claudin-5CLDN5AWALTMVCFTMDVCFCPETRL1BEC1Transmembrane protein deleted in VCFStransmembrane protein deleted in velocardiofacial syndrome

Drugs may aim to stabilize or enhance tight junction integrity via upregulation or stabilization of claudin-5, impacting vascular permeability and protecting the blood-brain barrier.