THE ROLE OF NADPH OXIDASE ACTIVATION IN URIC ACID-INDUCED PODOCYTE INJURY

Podocyte injury is a key event in the progression of hyperuricemia-related kidney diseases. Elevated uric acid levels induce oxidative stress, cytoskeletal disruption, and apoptosis in podocytes, leading to impaired glomerular filtration. NADPH oxidase has been identified as a major source of reactive oxygen species in podocytes, mediating oxidative damage and promoting cellular dysfunction. This thesis investigates the role of NADPH oxidase activation in uric acid-induced podocyte injury and explores the underlying molecular mechanisms. Understanding these pathways provides insight into potential therapeutic strategies to protect podocytes, reduce proteinuria, and prevent progression of chronic kidney disease. The study emphasizes the importance of targeting NADPH oxidase and oxidative stress in the management of hyperuricemia-associated renal disorders.