Cimolai Ozcan

ABSTRACT

Kidney function depends on the structural and physiological integrity of nephrons, which are highly susceptible to ischemic, toxic, inflammatory, and metabolic insults. Acute kidney injury (AKI) disrupts nephron architecture and impairs filtration, electrolyte balance, and waste elimination, often progressing to chronic kidney disease when tissue repair is incomplete. Increasing evidence indicates that successful nephron recovery is closely associated with metabolic reprogramming, enabling injured tubular epithelial cells to adapt to transient oxygen deprivation and energy deficiency. During the early stages of renal repair