Endothelial cell permeability regulation

Endothelial cell permeability regulation" is not a specific molecule or receptor but rather describes a complex physiological process by which the **endothelial monolayer** controls the passage of fluids, solutes, and cells between the bloodstream and surrounding tissues. This process is primarily governed by specialized protein complexes at intercellular junctions—most notably **adherens junctions** (such as those involving VE-cadherin)—and is dynamically modulated in response to mechanical and chemical stimuli[2][1]. The integrity and remodeling of these junctions are crucial for maintaining tissue–fluid balance; their dysfunction can lead to pathological leakage (hyperpermeability), contributing to conditions such as edema, inflammation, ARDS, systemic capillary leak syndrome, angioedema, anaphylaxis, diabetic eye diseases, and various CNS disorders[2][5]. Key molecular players include adherens junction proteins (e.g., VE-cadherin), cytoskeletal regulators (e.g., cortactin), signaling molecules like nitric oxide synthase (eNOS), protein kinases such as PKC and myosin light chain kinase[3], as well as transient receptor potential channels that mediate calcium influx during hyperpermeability responses[2]. Because this term refers to a regulatory mechanism rather than a discrete druggable target or single molecular entity, it should not be classified as a canonical therapeutic target.

Other names

Regulation of endothelial permeabilityEndothelial barrier functionVascular permeability regulation