ArticleNature communications2010
Mitochondrial respiration protects against oxygen-associated DNA damage.
Article in Nature communications, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 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
75 citing papers in PubMed, 140 citations in OpenAlex.
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- RANBP1 promotes oral cancer progression through activating YAP1 and NDUFB3 derived from the database of single-cell sequencing.Cancer cell international · 2026Article
- Article
- Hydrogen sulfide increases intracellular oxygen and inhibits the HIF response.The Journal of biological chemistry · 2026Article
- Bulk and Single-Cell Transcriptomics Reveal That SCO2 Drives Psoriasis via Activating CCR7International journal of molecular sciences · 2026Article
- Power and poison: The intersections of HThe Journal of biological chemistry · 2025Review
- Resolvin D1-mediated cellular crosstalk protects against MASH.JHEP reports : innovation in hepatology · 2025Article
- Inhibition and Rescue of Hyperglycemia-Induced Cellular Senescence by Mitochondrial Transfer from Enucleated Mesenchymal Stem Cell-Derived Microvesicles for Chronic Wound Healing.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mitochondrial Dysfunction in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.Physiology (Bethesda, Md.) · 2025Review
- Extra Virgin Olive Oil Phenolic Compounds: Modulating Mitochondrial Function and Protecting Against Chronic Diseases-A Narrative Review.Nutrients · 2025Review
- Lovastatin-Induced Mitochondrial Oxidative Stress Leads to the Release of mtDNA to Promote Apoptosis by Activating cGAS-STING Pathway in Human Colorectal Cancer Cells.Antioxidants (Basel, Switzerland) · 2024Article
- Mitochondrial respiratory function is preserved under cysteine starvation via glutathione catabolism in NSCLC.Nature communications · 2024Article
- Decoding the mitochondrial connection: development and validation of biomarkers for classifying and treating systemic lupus erythematosus through bioinformatics and machine learning.BMC rheumatology · 2023Article
- Review
- Label-free optical metabolic imaging of adipose tissues for prediabetes diagnosis.Theranostics · 2023Article
- Modulating gut dysbiosis and mitochondrial dysfunction in oxazolone-induced ulcerative colitis: the restorative effects of β-glucan and/or celastrol.Redox report : communications in free radical research · 2022Article
- Mitochondrial signal transduction.Cell metabolism · 2022Review
- Biochemical, Structural Analysis, and Docking Studies of Spiropyrazoline Derivatives.International journal of molecular sciences · 2022Article
- Mitochondrial complex IV defects induce metabolic and signaling perturbations that expose potential vulnerabilities in HCT116 cells.FEBS open bio · 2022Article
- Of the many cellular responses activated by TP53, which ones are critical for tumour suppression?Cell death and differentiation · 2022Review
15 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
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Oxygen is not only required for oxidative phosphorylation but also serves as the essential substrate for the formation of reactive oxygen species (ROS), which is implicated in ageing and tumorigenesis. Although the mitochondrion is known for its bioenergetic function, the symbiotic theory originally proposed that it provided protection against the toxicity of increasing oxygen in the primordial atmosphere. Using human cells lacking Synthesis of Cytochrome c Oxidase 2 (SCO2-/-), we have tested the oxygen toxicity hypothesis. These cells are oxidative phosphorylation defective and glycolysis dependent; they exhibit increased viability under hypoxia and feature an inverted growth response to oxygen compared with wild-type cells. SCO2-/- cells have increased intracellular oxygen and nicotinamide adenine dinucleotide (NADH) levels, which result in increased ROS and oxidative DNA damage. Using this isogenic cell line, we have revealed the genotoxicity of ambient oxygen. Our study highlights the importance of mitochondrial respiration both for bioenergetic benefits and for maintaining genomic stability in an oxygen-rich environment.
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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.