Validation experiment designed to validate causal mechanisms targeting RUBCN in PTEC-specific RUBCN knockout mice. Primary outcome: metabolic syndrome development and autophagy flux changes
Generated and characterized proximal tubular epithelial cell (PTEC)-specific RUBCN-deficient knockout (KO) mice to investigate the physiological role of RUBCN in kidney function. The study examined autophagy flux in PTECs and tested protection against acute ischemic kidney injury. Unexpectedly, KO mice developed metabolic syndrome features with expanded lysosomes containing multi-layered phospholipids in PTECs, despite enhanced autophagy. The research revealed that sustained high autophagic flux leads to mobilization of phospholipids from cellular membranes to lysosomes, contributing to systemic metabolic dysfunction.
Generation of tissue-specific knockout mice, histological analysis of kidney tissue, metabolic profiling, assessment of autophagy markers, ischemia-reperfusion injury testing
Protection from kidney injury due to enhanced autophagy
Increased autophagy flux and protection from ischemic injury
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