Abstract: The kidney is a highly metabolic organ, especially the proximal renal tubular epithelial cells, which mainly rely on fatty acid oxidation for energy supply under physiological conditions. However, when acute kidney injury (AKI) occurs, mitochondrial and peroxisome dysfunction causes metabolic reprogramming of proximal renal tubular epithelial cells, and the energy supply turns to glycolysis and lactate production, accompanied by fatty acid oxidation disorder and impaired gluconeogenesis. Metabolic reprogramming may be a beneficial energy compensation for kidney in the short term. However, this process also aggravates kidney damage. This article reviews the role of metabolic reprogramming of proximal renal tubular epithelial cells in AKI.

Key words: acute kidney injury, metabolic reprogramming, proximal renal tubular epithelial cells