期刊
ANTIOXIDANTS
卷 11, 期 7, 页码 -出版社
MDPI
DOI: 10.3390/antiox11071356
关键词
acute kidney injury; chronic kidney disease; mitochondria; oxidative stress; PGC-1 alpha
资金
- FIS/Fondos FEDER [PI18/01366, PI19/00588, PI19/00815, DTS18/00032, PI21/00251, PI20/000140, AC18/00064, AC18/00071, PMP21/00109, RD016/0009]
- Sociedad Espanola de Nefrologia, FRIAT, Comunidad de Madrid en Biomedicina [B2017/BMD-3686 CIFRA2-CM]
- Instituto de Salud Carlos III (ISCIII) [RICORS2040 (RD21/0005/0001)]
- Financiado por la Union Europea-NextGenerationEU
- Mecanismo para la Recuperacion y la Resiliencia (MRR)
- ISCIII PFIS
- Ramon y Cajal program
- MICIU
- FEBS Long-Term Fellowship
Acute kidney injury (AKI) and chronic kidney disease (CKD) are interconnected conditions, and mitochondrial dysfunction and oxidative stress play important roles in the progression of both diseases. New therapeutic approaches targeting mitochondria are needed, but there are barriers to clinical development, such as the lack of diagnostic tests for renal mitochondrial dysfunction.
Acute kidney injury (AKI) and chronic kidney disease (CKD) are interconnected conditions, and CKD is projected to become the fifth leading global cause of death by 2040. New therapeutic approaches are needed. Mitochondrial dysfunction and oxidative stress have emerged as drivers of kidney injury in acute and chronic settings, promoting the AKI-to-CKD transition. In this work, we review the role of mitochondrial dysfunction and oxidative stress in AKI and CKD progression and discuss novel therapeutic approaches. Specifically, evidence for mitochondrial dysfunction in diverse models of AKI (nephrotoxicity, cytokine storm, and ischemia-reperfusion injury) and CKD (diabetic kidney disease, glomerulopathies) is discussed; the clinical implications of novel information on the key role of mitochondria-related transcriptional regulators peroxisome proliferator-activated receptor gamma coactivator 1-alpha, transcription factor EB (PGC-1 alpha, TFEB), and carnitine palmitoyl-transferase 1A (CPT1A) in kidney disease are addressed; the current status of the clinical development of therapeutic approaches targeting mitochondria are updated; and barriers to the clinical development of mitochondria-targeted interventions are discussed, including the lack of clinical diagnostic tests that allow us to categorize the baseline renal mitochondrial dysfunction/mitochondrial oxidative stress and to monitor its response to therapeutic intervention. Finally, key milestones for further research are proposed.
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