Claudin-17 Deficiency in Mice Results in Kidney Injury Due to Electrolyte Imbalance and Oxidative Stress.

The multi-gene claudin () family of tight junction proteins have isoform-specific roles in blood-tissue barrier regulation. , a putative anion pore-forming based on its structural characterization, is assumed to regulate anion balance across the blood-tissue barriers. However, our knowledge about in physiology and pathology is limited. The current study investigated how deficiency in mice affects blood electrolytes and kidney structure. mice revealed no breeding abnormalities, but the newborn pups exhibited delayed growth. Adult mice displayed electrolyte imbalance, oxidative stress, and injury to the kidneys. Ingenuity pathway analysis followed by RNA-sequencing revealed hyperactivation of signaling pathways and downregulation of SOD1 expression in kidneys associated with inflammation and reactive oxygen species generation, demonstrating the importance of in the maintenance of electrolytes and reactive oxygen species across the blood-tissue barrier.