ArticleProceedings of the National Academy of Sciences of the United States of America1999
Mitochondrial disease in superoxide dismutase 2 mutant mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 187 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
187 citing papers in PubMed, 581 citations in OpenAlex.
- Seizure and redox rescue in a model of glucose transport deficiency.PLoS computational biology · 2025Article
- Targeting oxidative stress-induced lipid peroxidation enhances podocyte function in cystinosis.Journal of translational medicine · 2025Article
- Impacts of mitochondrial dysfunction on axonal microtubule bundles as a potential mechanism of neurodegeneration.Frontiers in neuroscience · 2025Review
- Research progress on DNA hydroxymethylation in atrial fibrillation: a review.Frontiers in pharmacology · 2025Review
- The associations between oxidative stress and epilepsy: a bidirectional two-sample Mendelian randomization study.Acta epileptologica · 2024Article
- Mitochondrial Reactive Oxygen Species Dysregulation in Heart Failure with Preserved Ejection Fraction: A Fraction of the Whole.Antioxidants (Basel, Switzerland) · 2024Review
- Mitochondrial antioxidants abate SARS-COV-2 pathology in mice.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Mitochondrial impairment, decreased sirtuin activity and protein acetylation in dorsal root ganglia in Friedreich Ataxia models.Cellular and molecular life sciences : CMLS · 2023Article
- Lysophosphatidylcholine-DHA Specifically Induces Cytotoxic Effects of the MDA-MB-231 Human Breast Cancer Cell LineNutrients · 2023Article
- Interactions of reactive sulfur species with metalloproteins.Redox biology · 2023Review
- Iturin A Strongly Inhibits the Growth and T-2 Toxin Synthesis ofFoods (Basel, Switzerland) · 2023Article
- Role of Protein Damage Inflicted by Dopamine Metabolites in Parkinson's Disease: Evidence, Tools, and Outlook.Chemical research in toxicology · 2022Review
- NADPH Oxidase Mediates Oxidative Stress and Ventricular Remodeling through SIRT3/FOXO3a Pathway in Diabetic Mice.Antioxidants (Basel, Switzerland) · 2022Article
- A CRISPR screen identifies redox vulnerabilities for KEAP1/NRF2 mutant non-small cell lung cancer.Redox biology · 2022Article
- In Silico Identification of Novel Inhibitors Targeting the Homodimeric Interface of Superoxide Dismutase from the Dental PathogenAntioxidants (Basel, Switzerland) · 2022Article
- Genome-wide screening in the haploid system reveals Slc25a43 as a target gene of oxidative toxicity.Cell death & disease · 2022Article
- Mitochondrial Management of Reactive Oxygen Species.Antioxidants (Basel, Switzerland) · 2021Review
- Reactive Oxygen Species in Acute Lymphoblastic Leukaemia: Reducing Radicals to Refine Responses.Antioxidants (Basel, Switzerland) · 2021Review
- Neuron-specific mitochondrial oxidative stress results in epilepsy, glucose dysregulation and a striking astrocyte response.Neurobiology of disease · 2021Article
- Functions of ROS in Macrophages and Antimicrobial Immunity.Antioxidants (Basel, Switzerland) · 2021Review
127 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
13 authors at 5 institutions in 1 country.
Funding
Abstract
Oxidative stress has been implicated in many diseases. The chief source of reactive oxygen species within the cell is the mitochondrion. We have characterized a variety of the biochemical and metabolic effects of inactivation of the mouse gene for the mitochondrial superoxide dismutase (CD1-Sod2(tm1Cje)). The Sod2 mutant mice exhibit a tissue-specific inhibition of the respiratory chain enzymes NADH-dehydrogenase (complex I) and succinate dehydrogenase (complex II), inactivation of the tricarboxylic acid cycle enzyme aconitase, development of a urine organic aciduria in conjunction with a partial defect in 3-hydroxy-3-methylglutaryl-CoA lyase, and accumulation of oxidative DNA damage. These results indicate that the increase in mitochondrial reactive oxygen species can result in biochemical aberrations with features reminiscent of mitochondrial myopathy, Friedreich ataxia, and 3-hydroxy-3-methylglutaryl-CoA lyase deficiency.
Indexed as
Identifiers
What OpenQuestion holds
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.