ArticleGenetics2023
Mitochondrial superoxide dismutase Sod2 suppresses nuclear genome instability during oxidative stress.
Article in Genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Cosmetogenomics unveiled: a systematic review of AI, genomics, and the future of personalized skincare.Frontiers in artificial intelligence · 2025Pooled it
- Research Progress of Cuproptosis in Orthopaedics: Opportunities and Challenges.Journal of cellular and molecular medicine · 2026Review
- Less Is More: A Physiological Dose of Vitamin B12 Enhances Neural Recovery Compared to a High Dose in an H₂O₂-Stressed SH-SY5Y Neural-Like Cell Model.Molecular neurobiology · 2026Article
- The oxidative cost of losing low temperature viability protein 1 [Ltv1]: insights into cellular damage and homeostasis.FEMS yeast research · 2026Article
- The curious life of human mitochondrial SOD2.International journal of biological macromolecules · 2026Review
- Boric acid and quercetin supplementations alleviated paraquat-induced neurotoxic and irritation effects in human SH-SY5Y cells and in ovo models.BMC complementary medicine and therapies · 2025Article
- Gene and metabolite changes triggered by downregulation of JUNB and ZNF281 in idiopathic pulmonary arterial hypertension: potential mechanisms revealed by multi-omics study.Translational pediatrics · 2025Article
- Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025Review
- Mitochondrial Complex Member VdNuo1 Recruits Superoxide Dismutases VdSOD2/4 to Maintain Superoxide Anion Homeostasis During Pathogenesis in Verticillium dahliae.Molecular plant pathology · 2025Article
- The Role of Oxidative Stress-Related Gene Polymorphisms (Medicina (Kaunas, Lithuania) · 2025Article
- The Role of Redox Environment in Tumors.Current medicinal chemistry · 2025Review
- Gut microbiota and colorectal cancer: mechanistic insights, diagnostic advances, and microbiome-based therapeutic strategies.Frontiers in microbiology · 2025Review
- The Key Enzymes of Carbon Metabolism and the Glutathione Antioxidant System ProtectJournal of fungi (Basel, Switzerland) · 2024Article
- Early oxidative stress and DNA damage in Aβ-burdened hippocampal neurons in an Alzheimer's-like transgenic rat model.Communications biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Oxidative stress can damage DNA and thereby contribute to genome instability. To avoid an imbalance or overaccumulation of reactive oxygen species (ROS), cells are equipped with antioxidant enzymes that scavenge excess ROS. Cells lacking the RecQ-family DNA helicase Sgs1, which contributes to homology-dependent DNA break repair and chromosome stability, are known to accumulate ROS, but the origin and consequences of this oxidative stress phenotype are not fully understood. Here, we show that the sgs1 mutant exhibits elevated mitochondrial superoxide, increased mitochondrial mass, and accumulation of recombinogenic DNA lesions that can be suppressed by antioxidants. Increased mitochondrial mass in the sgs1Δ mutant is accompanied by increased mitochondrial branching, which was also inducible in wildtype cells by replication stress. Superoxide dismutase Sod2 genetically interacts with Sgs1 in the suppression of nuclear chromosomal rearrangements under paraquat (PQ)-induced oxidative stress. PQ-induced chromosome rearrangements in the absence of Sod2 are promoted by Rad51 recombinase and the polymerase subunit Pol32. Finally, the dependence of chromosomal rearrangements on the Rev1/Pol ζ mutasome suggests that under oxidative stress successful DNA synthesis during DNA break repair depends on translesion DNA synthesis.
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.