OCLN (occludin) is an integral tight junction protein with critical roles in maintaining epithelial and endothelial barriers. Structurally, occludin contains a MARVEL domain essential for its function 1. Primary functions include regulating paracellular transport and serving as an HCV coreceptor in hepatocytes [UniProt]. Beyond structural barrier roles, occludin regulates apoptosis by enhancing caspase-3 transcription, with inflammation-induced occludin downregulation paradoxically limiting epithelial apoptosis in gastrointestinal disease 2. OCLN expression is downregulated by T helper 2 cytokines (IL-4/IL-13) via STAT6 phosphorylation in atopic dermatitis, impairing skin barrier function 3. During sepsis-induced lung injury, microRNA-193b-5p suppresses occludin expression, reducing endothelial barrier integrity; MSC therapy counteracts this through miR-193b-5p inhibition 4. Pathologically, Streptococcus pneumoniae induces occludin degradation through autophagy via bacterial StkP-mediated BECN1 phosphorylation, compromising the alveolar epithelial barrier 5. OCLN variants cause pseudo-TORCH syndrome 1, characterized by developmental delay, polymicrogyria, and epilepsy 6. In cancer, occludin is typically downregulated and serves as a prognostic biomarker inversely correlating with tumor progression in renal cell carcinoma 7. These findings establish OCLN as a multifunctional protein governing both barrier integrity and immunoregulatory processes.