ReviewAntioxidants (Basel, Switzerland)2022
Tubular Mitochondrial Dysfunction, Oxidative Stress, and Progression of Chronic Kidney Disease.
Review in Antioxidants (Basel, Switzerland), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
What it found
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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
73 citing papers in PubMed, 100 citations in OpenAlex.
- Frailty index and type 2 diabetes with renal complications: insights from Mendelian randomization and retrospective observational study.Renal failure · 2026Observational
- Pharmacological activation of SIRT1 alleviates sepsis-associated acute kidney injury by improving renal mitochondrial energy metabolism.Renal failure · 2026Article
- Oxidative Stress and Mitochondrial Dysfunction in Chronic Kidney Disease: From Molecular Mechanisms to Biomarkers and Targeted Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Renoprotective Effects of a Herbal Formulation Against Lipopolysaccharide-Induced Acute Kidney Injury Through Anti-Inflammatory and Antioxidant Activities.Life (Basel, Switzerland) · 2026Article
- Review
- Morin attenuates vancomycin-induced nephrotoxicity via Nrf-2/HO-1, SIRT1/PGC1α and AKT/FOXO1A pathways.Molecular biology reports · 2026Article
- Mechanisms of Obesity-Related Kidney Disease: From Adipose Depot Biology to the Chymase-Aldosterone and Ghrelin-Leptin Axes.Biomolecules · 2026Review
- Redox-Mediated Mitochondrial Dysfunction as a Common Pathogenic Axis in Acute Kidney Injury and Chronic Kidney Disease.Biomolecules · 2026Review
- Review
- Article
- Redox control at the ER-mitochondria interface in kidney transplantation: MAM-centered stress signaling and translational organoid platforms.Redox biology · 2026Review
- From AKI to CKD mechanisms of maladaptive repair and disease progression.International urology and nephrology · 2026Review
- The role of protein prenylation in kidney diseases: Molecular basis and therapeutic implications.Molecular biology reports · 2026Review
- Beyond the Cell Atlas: Functional Communities as the Essential Pathologic Units Driving Kidney Disease.Journal of the American Society of Nephrology : JASN · 2026Review
- Molecular and Genetic Determinants of Nephrocalcinosis: Mechanisms, Genotype-Phenotype Correlations, and Precision Medicine.International journal of molecular sciences · 2026Review
- Alterations in mitochondria and cellular senescence in aged sEH null female kidneys.GeroScience · 2026Article
- Oxidative Stress-Driven Mechanisms and Biomarkers of Drug-Induced Nephrotoxicity: Translational Insights and Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2026Review
- miR-4516-Loaded Engineered Milk Extracellular Vesicles Attenuate Indoxyl Sulfate-Induced Mitochondrial Dysfunction and Improve Renal Function in a CKD Mouse Model.International journal of molecular sciences · 2026Article
- Hypertension-Induced Renal Injury: From Pathophysiology to Therapeutic Perspectives.Biomedicines · 2026Review
- L-Carnitine, a new biomarker screened based on untargeted metabolomics, predict cardiac surgery-associated acute kidney injury: a prospective cohort study.BMC nephrology · 2026Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
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-1α, 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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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.