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Abstract
Chronic kidney disease (CKD) is associated with dysregulated lipid metabolism, particularly in proximal kidney tubules.
- Proximal tubules primarily rely on fatty acid oxidation for energy rather than glycolysis, which is reflected by the absence of key glycolytic enzymes.
- Maladaptive hypertrophy occurs in CKD as surviving nephrons compensate to maintain kidney function.
- PPARα is identified as a key regulator of proximal tubule cell size and compensatory hypertrophy.
- Decreased AMPK activity in CKD impairs cellular responses to energy stress, as shown by altered AMP/ATP ratios.
- Uremic metabolites may worsen defective energy sensing by reducing AMPK function.
- ULK1 regulates AMPK activity by enhancing its sensitivity to AMP through specific phosphorylation sites.
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