Validation experiment designed to validate causal mechanisms targeting RUBCN in PTEC-specific RUBCN knockout mice. Primary outcome: autophagy flux and metabolic syndrome development
Generated proximal tubular epithelial cell (PTEC)-specific RUBCN-deficient knockout mice to investigate the physiological role of RUBCN in kidney cells. Analyzed the phenotype including autophagy flux, kidney injury protection, and metabolic parameters. Found that despite sustained high autophagic flux in PTECs, KO mice were not protected from acute ischemic kidney injury. Unexpectedly, KO mice developed features of metabolic syndrome with expanded lysosomes containing multi-layered phospholipids in PTECs.
Generated conditional knockout mice with PTEC-specific RUBCN deletion, performed ischemia-reperfusion injury models, analyzed metabolic parameters and lysosomal morphology
Expected protection from kidney injury due to enhanced autophagy
Measurement of autophagic flux markers, kidney injury parameters, and metabolic syndrome features
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