Abstract: Acute kidney injury (AKI) is a systemic clinic syndrome increasing morbidity and mortality worldwide in recent years. Mitophagy plays a prominent role in reactive oxygen species elimination, energy metabolism, inhibiting inflammation, and mitochondrial dynamics hemostasis by engulfing injured and dysfunctional mitochondria. Experimental studies have shown that mitophagy deficiency promotes renal tubular epithelial damage and renal function decreasing in AKI induced by ischemia reperfusion injury, cisplatin, contrast agents and sepsis. The review will introduce the protective role of mitophagy in AKI, which may serve as novel therapeutic targets for the development of potential therapies to improve AKI prognosis.

Key words: mitophagy, acute kidney injury, reactive oxygen species, inflammation