ReviewJournal of the American Society of Nephrology : JASN2017
Pharmacologic Approaches to Improve Mitochondrial Function in AKI and CKD.
Review in Journal of the American Society of Nephrology : JASN, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
108 citing papers in PubMed, 211 citations in OpenAlex.
- Eight weeks of MitoQ supplementation does not alter kidney function or urinary kidney injury biomarkers in middle-aged and older adults.American journal of physiology. Renal physiology · 2026Trial
- Acute high-dose MitoQ does not increase urinary kidney injury markers in healthy adults: a randomized crossover trial.American journal of physiology. Renal physiology · 2024Trial
- Methylcrotonyl-CoA carboxylase 2 supports leucine catabolism to promote mitochondrial biogenesis and alleviate cisplatin-induced acute kidney injury.Kidney research and clinical practice · 2026Article
- Renal function-improving action of Pentadecyl®, a multifunctional triglyceride fromExperimental and therapeutic medicine · 2026Article
- Extracellular Vesicles as Mediators of Endothelial and Tubular Injury in Cardiac Surgery-Associated Acute Kidney Injury.Biomedicines · 2026Review
- Article
- Dihydromyricetin protects against cisplatin-induced renal injury and mitochondria-mediated apoptosis via the EGFR/HSP27/STAT3 signaling pathway.Renal failure · 2025Article
- Integration of mitochondrial gene expression and immune landscape in acute kidney injury prediction.Renal failure · 2025Article
- Long-Term Functional and Structural Renoprotection After Experimental Acute Kidney Injury in Subclinical Chronic Kidney Disease In Vivo.International journal of molecular sciences · 2025Article
- Article
- Article
- Chymase Inhibition Attenuates Kidney Fibrosis in a Chronic Mouse Model of Renal Ischemia-Reperfusion Injury.International journal of molecular sciences · 2025Article
- Assays to enhance metabolic phenotyping in the kidney.American journal of physiology. Renal physiology · 2025Article
- Long-Term Physical Exercise for Preventing CKD in Older Adults: A Randomized Clinical Trial.Journal of the American Society of Nephrology : JASN · 2025Article
- Twist2 knockdown alleviates renal ischemia-reperfusion injury by maintaining mitochondrial function and enhancing mitophagy through Bnip3.Human cell · 2025Article
- Tubular MYDGF Slows Progression of Chronic Kidney Disease by Maintaining Mitochondrial Homeostasis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Transformation of acute kidney injury to chronic kidney disease: the interaction between mitophagy and NLRP3 inflammasome.Frontiers in molecular biosciences · 2025Review
- α-Mangostin prevents diabetic cardiomyopathy by inhibiting oxidative damage and lipotoxicity through the AKT-FOXO1-CD36 pathway.Frontiers in pharmacology · 2025Article
- Preventive Effects of Resistance Training on Hemodynamics and Kidney Mitochondrial Bioenergetic Function in Ovariectomized Rats.International journal of molecular sciences · 2024Article
- Exploring the role and therapeutic potential of lipid metabolism in acute kidney injury.Renal failure · 2024Review
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
AKI is associated with high morbidity and mortality, and it predisposes to the development and progression of CKD. Novel strategies that minimize AKI and halt the progression of CKD are urgently needed. Normal kidney function involves numerous different cell types, such as tubular epithelial cells, endothelial cells, and podocytes, working in concert. This delicate balance involves many energy-intensive processes. Fatty acids are the preferred energy substrates for the kidney, and defects in fatty acid oxidation and mitochondrial dysfunction are universally involved in diverse causes of AKI and CKD. This review provides an overview of ATP production and energy demands in the kidney and summarizes preclinical and clinical evidence of mitochondrial dysfunction in AKI and CKD. New therapeutic strategies targeting mitochondria protection and cellular bioenergetics are presented, with emphasis on those that have been evaluated in animal models of AKI and CKD. Targeting mitochondrial function and cellular bioenergetics upstream of cellular damage may offer advantages compared with targeting downstream inflammatory and fibrosis processes.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.