ReviewFree radical biology & medicine2015
Oxidative stress in inherited mitochondrial diseases.
Review in Free radical biology & medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05483738 (The Impact of Mitochondrial Dysfunction on Human Bone Cell Metabolism and Remodelling), which is not on this map. Cited by 71 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.
The Impact of Mitochondrial Dysfunction on Human Bone Cell Metabolism and Remodelling
Who cites it
71 citing papers in PubMed, 146 citations in OpenAlex.
- Randomized dose-escalation trial of elamipretide in adults with primary mitochondrial myopathy.Neurology · 2018Trial
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- Neuronal branching in stem cell models of mitochondrial and neurological diseases.Stem cells (Dayton, Ohio) · 2025Review
- Mitochondrial DNA Dysfunction in Cardiovascular Diseases: A Novel Therapeutic Target.Antioxidants (Basel, Switzerland) · 2025Review
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- Vitamin A treatment restores vision failures arising from Leber's hereditary optic neuropathy-linked mtDNA mutation.JCI insight · 2025Article
- Mitochondrial diseases: from molecular mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Alleviating D-Galactose-Induced Aging in Mice by Modulating Gut-Liver Axis UsingFoods (Basel, Switzerland) · 2024Article
- Arginine Supplementation in MELAS Syndrome: What Do We Know about the Mechanisms?International journal of molecular sciences · 2024Review
- Optimized allotopic expression of mitochondrial ND6 transgene restored complex I and apoptosis deficiencies caused by LHON-linked ND6 14484T > C mutation.Journal of biomedical science · 2023Article
- Oxidative Stress: A Suitable Therapeutic Target for Optic Nerve Diseases?Antioxidants (Basel, Switzerland) · 2023Review
- Identification of peripheral vascular function measures and circulating biomarkers of mitochondrial function in patients with mitochondrial disease.Clinical and translational science · 2023Article
- Real-Time Measurement of the Mitochondrial Bioenergetic Profile of Neutrophils.Journal of visualized experiments : JoVE · 2023Article
- A narrative review of the mechanisms and consequences of intermittent hypoxia and the role of advanced analytic techniques in pediatric autonomic disorders.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2023Review
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- The bridge between cell survival and cell death: reactive oxygen species-mediated cellular stress.EXCLI journal · 2023Review
- Chenodeoxycholic Acid (CDCA) Promoted Intestinal Epithelial Cell Proliferation by Regulating Cell Cycle Progression and Mitochondrial Biogenesis in IPEC-J2 Cells.Antioxidants (Basel, Switzerland) · 2022Article
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- Natural Antioxidant Compounds as Potential Pharmaceutical Tools against Neurodegenerative Diseases.ACS omega · 2022Review
11 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondria are a source of reactive oxygen species (ROS). Mitochondrial diseases are the result of inherited defects in mitochondrially expressed genes. One potential pathomechanism for mitochondrial disease is oxidative stress. Oxidative stress can occur as the result of increased ROS production or decreased ROS protection. The role of oxidative stress in the five most common inherited mitochondrial diseases, Friedreich ataxia, LHON, MELAS, MERRF, and Leigh syndrome (LS), is discussed. Published reports of oxidative stress involvement in the pathomechanisms of these five mitochondrial diseases are reviewed. The strongest evidence for an oxidative stress pathomechanism among the five diseases was for Friedreich ataxia. In addition, a meta-analysis was carried out to provide an unbiased evaluation of the role of oxidative stress in the five diseases, by searching for "oxidative stress" citation count frequency for each disease. Of the five most common mitochondrial diseases, the strongest support for oxidative stress is for Friedreich ataxia (6.42%), followed by LHON (2.45%), MELAS (2.18%), MERRF (1.71%), and LS (1.03%). The increased frequency of oxidative stress citations was significant relative to the mean of the total pool of five diseases (p<0.01) and the mean of the four non-Friedreich diseases (p<0.0001). Thus there is support for oxidative stress in all five most common mitochondrial diseases, but the strongest, significant support is for Friedreich ataxia.
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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.