Cathepsin B regulates renal urate transport via glycolysis in hyperuricemia
Hyperuricemia (HUA) is a prevalent metabolic disorder primarily caused by impaired renal uric acid excretion. In this study, we investigated the role of cathepsin B (CTSB) in regulating renal urate transport and metabolism. Using renal proximal tubular epithelial cell-specific CTSB knockout mice, RNA sequencing revealed that CTSB deficiency led to downregulation of glycolysis-related genes and restoration of urate transporter expression patterns, promoting uric acid excretion and reducing systemic inflammation. This dataset provides transcriptomic insights into the molecular mechanisms by which CTSB contributes to renal uric acid handling during HUA and highlights CTSB as a potential therapeutic target.