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Mitochondrial Dysfunction in Acute Kidney Injury: Intersections Between Chemotherapy and Novel Cancer Immunotherapies
Zaroon Zaroon1, Carlotta D'Ambrosio1, Filomena de Nigris1
1Department of Precision Medicine, University of Campania "Luigi Vanivtelli", 80138 Naples, Italy.
Abstract:
Acute kidney injury (AKI) remains a major clinical challenge, with high morbidity and limited therapeutic options. In recent years, mitochondria have gained considerable attention as key regulators of the metabolic and immune responses during renal injury. Beyond their classical role in ATP production, mitochondria participate directly in inflammatory signaling, releasing mitochondrial DNA and other DAMPs that activate pathways such as TLR9, cGAS-STING, and the NLRP3 inflammasome. At the same time, immune cells recruited to the kidney undergo significant metabolic shifts that influence whether injury progresses or resolves. Increasing evidence also shows that immune-modulating therapies, including immune checkpoint inhibitors and innovative cell-based immunotherapies, can influence mitochondrial integrity, thereby altering renal susceptibility to injury. This review first summarizes the established knowledge on mitochondrial dysfunction in AKI, with emphasis on distinct mechanistic pathways activated by chemotherapy and immunotherapy. It then discusses emerging mitochondrial-targeted therapeutic strategies, logically integrating preclinical insights with data from ongoing and proposed clinical trials to present a coherent translational outlook.
Insights
Mitochondria play a key role in acute kidney injury (AKI) by regulating immune and metabolic responses. Targeting mitochondria offers promising therapeutic strategies for AKI, integrating preclinical and clinical findings.
Area of Science:
- Nephrology
- Immunology
- Mitochondrial Biology
Background:
- Acute kidney injury (AKI) presents significant clinical challenges with limited treatments.
- Mitochondria are increasingly recognized as central regulators of metabolic and immune responses in renal injury.
- Mitochondrial dysfunction contributes to AKI pathogenesis through inflammatory signaling and altered immune cell metabolism.
Purpose of the Study:
- To review the role of mitochondrial dysfunction in AKI, focusing on chemotherapy and immunotherapy.
- To discuss emerging mitochondrial-targeted therapeutic strategies for AKI.
- To provide a translational outlook by integrating preclinical and clinical data.
Main Methods:
- Literature review of established knowledge on mitochondrial dysfunction in AKI.
- Emphasis on mechanistic pathways activated by chemotherapy and immunotherapy.
- Discussion of emerging mitochondrial-targeted therapies and clinical trial data.
Main Results:
- Mitochondria actively participate in inflammatory signaling during AKI via DAMP release and pathway activation (e.g., TLR9, cGAS-STING, NLRP3).
- Immune cell metabolic shifts influence AKI progression or resolution.
- Immunotherapies can impact mitochondrial integrity and renal injury susceptibility.
Conclusions:
- Mitochondrial dysfunction is a critical factor in AKI development and progression.
- Mitochondrial-targeted therapies represent a promising avenue for AKI treatment.
- Further research integrating preclinical and clinical data is crucial for therapeutic advancement.
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