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Mitochondrial homeostasis imbalance in renal ischemia-reperfusion injury: Mechanisms and Targeted Interventions

biochemistry
molecular-biology
nephrology
urology

Abstract

Renal ischemia-reperfusion injury (RIRI) constitutes a key pathological basis for acute kidney injury and transplant dysfunction, with its core mechanisms closely linked to mitochondrial damage. Mitochondria serve not only as the central hub for energy metabolism and redox reactions but also play critical roles in maintaining calcium homeostasis, regulating apoptosis, and modulating inflammatory responses. This systematic review examines the structural and functional characteristics of mitochondria in RIRI, emphasizing the mitochondrial dysfunction induced by RIRI. This dysfunction encompasses ATP depletion, reactive oxygen species (ROS) accumulation, calcium overload, and loss of membrane potential, ultimately leading to apoptosis and necrosis of renal tubular epithelial cells. Mitochondrial quality control mechanisms—including biogenesis, dynamics, and autophagy—serve as critical pathways for maintaining mitochondrial homeostasis and defending against injury. This review systematically summarizes recent advances in mitochondrial dysfunction and quality control in RIRI, explores potential therapeutic strategies, and provides a theoretical basis for developing targeted mitochondrial interventions.
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