ReviewFrontiers in physiology2021
Mitochondrial Reactive Oxygen Species and Their Contribution in Chronic Kidney Disease Progression Through Oxidative Stress.
Review in Frontiers in physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 231 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
231 citing papers in PubMed, 368 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
- PROGRESS Study: Longitudinal analysis of antioxidant status and its relationship with heat shock proteins in children with chronic kidney disease.Pediatric nephrology (Berlin, Germany) · 2026Article
- Resveratroloside alleviates senescence-associated phenotypes in vitro through the coordinated regulation of mitochondrial function and chromatin structure.Biogerontology · 2026Article
- Cardiovascular-kidney-metabolic syndrome as a mitochondrial systems disorder.Nature reviews. Nephrology · 2026Review
- Translational Pharmaceutical Perspectives on Quinones as Antioxidant and Antidiabetic Agents in Diabetes and Its Complications.Pharmaceutics · 2026Review
- Dissipation of the mitochondrial proton motive force drives sepsis pathogenesis and explains hyperlactatemia's predictive value in sepsis mortality.World journal of critical care medicine · 2026Review
- Molecular Hydrogen and the Uremic Skeleton: A Critical Review and Turnover-State-Dependent Redox Hypothesis in CKD-MBD.Antioxidants (Basel, Switzerland) · 2026Review
- Oxidative Stress and Mitochondrial Dysfunction in Chronic Kidney Disease: From Molecular Mechanisms to Biomarkers and Targeted Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Synthetic Cyclic CAntioxidants (Basel, Switzerland) · 2026Article
- The Scavenger Function of LSECs, a Regulator of Liver Diseases.Current issues in molecular biology · 2026Review
- A new paradigm in Parkinson's disease: kidney-origin α-synuclein pathology driven by PKC signaling and aurothioglucose.Inflammopharmacology · 2026Review
- AGEs-RAGE Axis and Mitochondrial-Derived Peptides in Advanced Chronic Kidney Disease: Interconnected Pathways Beyond Inflammation and Nutrition.Antioxidants (Basel, Switzerland) · 2026Article
- Diet-Associated Regulation of Cardiac Metabolism: Molecular Determinants and Pathophysiological Consequences.Nutrients · 2026Review
- Redox Homeostasis, Metabolic Pathways and Plasticity in Uveal Melanoma Compared to Other Cancers.Cancers · 2026Review
- Review
- Polystyrene Nanoplastics Induce Early Mitochondrial Dysfunction in H9c2 Cardiomyoblasts Without Substantial Cell Damage.Antioxidants (Basel, Switzerland) · 2026Article
- Mitochondria: The Crossroads of Complement Activation and Kidney Injury Progression.International journal of molecular sciences · 2026Review
- Designed Liquid Crystalline Nanoassemblies From Clinically Validated Polyunsaturated Lipids for Combined Antioxidant, Anti-Apoptotic, and Neurotrophic Treatments.Advanced healthcare materials · 2026Article
- Oxidative stress-mediated DNA fragmentation involved in STING-dependent apoptosis in human keratinocytes by 5-amino-2-methylphenol under ambient UVB exposure.Archives of toxicology · 2026Article
171 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
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondria are known to generate approximately 90% of cellular reactive oxygen species (ROS). The imbalance between mitochondrial reactive oxygen species (mtROS) production and removal due to overproduction of ROS and/or decreased antioxidants defense activity results in oxidative stress (OS), which leads to oxidative damage that affects several cellular components such as lipids, DNA, and proteins. Since the kidney is a highly energetic organ, it is more vulnerable to damage caused by OS and thus its contribution to the development and progression of chronic kidney disease (CKD). This article aims to review the contribution of mtROS and OS to CKD progression and kidney function deterioration.
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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.