Advances in the Study of Mitophagy in Renal Ischemia–Reperfusion Injury

Abstract

Renal ischemia–reperfusion injury (IRI) is a leading etiology of acute kidney injury (AKI), predominantly observed in complex cardiovascular surgeries, severe traumatic shock, and renal transplantation. Oxidative stress, calcium overload, mitochondrial dysfunction, autophagy, and apoptosis are closely associated with renal IRI. Mitochondria not only serve as critical organelles for cellular oxidative respiration and energy production but also play vital roles in various biochemical processes including calcium homeostasis, signal transduction, energy metabolism, cell differentiation, apoptosis, renal ischemia, and reinjury. One particular form of autophagy, mitophagy, can accurately eliminate damaged or defective mitochondria, thereby maintaining mitochondrial homeostasis and playing a key role in renal IRI. To give a new approach to mechanistic research and clinical prevention and therapy of renal ischemia–reperfusion injury, this paper examines the key signaling pathways and novel therapeutic targets of mitophagy in ischemia–reperfusion injury.