ArticleNucleic acids research2018
Oxidative stress increases M1dG, a major peroxidation-derived DNA adduct, in mitochondrial DNA.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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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.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- The Oxidative DNA Lesion 6-Oxo-M1dG is a Potent Replication Block, Inducing Deletions and Base Substitution Mutations In Vivo.Chemical research in toxicology · 2026Article
- Diagnostic and therapeutic innovations in myocardial infarction: a focus on mitochondrial dysfunction.Frontiers in cardiovascular medicine · 2026Review
- Signaling pathways and targeted therapy for pulmonary hypertension.Signal transduction and targeted therapy · 2025Review
- ALDH1A1 in breast cancer: A prospective target to overcome therapy resistance (Review).Oncology letters · 2025Review
- Burden of pulmonary arterial hypertension in children globally, regionally, and nationally (1990-2021): results from the global burden of disease study.Frontiers in pediatrics · 2025Article
- Base-Displaced Intercalated Structure of the 3-(2-Deoxy-β-D-erythropentofuranosyl)-pyrimido[1,2-Chemical research in toxicology · 2023Article
- Accumulation of 8-oxodG within the human mitochondrial genome positively associates with transcription.NAR genomics and bioinformatics · 2023Article
- Metabolic reprogramming, oxidative stress, and pulmonary hypertension.Redox biology · 2023Review
- Quantitative estimation of intracellular oxidative stress in human tissues.Briefings in bioinformatics · 2022Article
- Cruciferous Vegetable Intake and Bulky DNA Damage within Non-Smokers and Former Smokers in the Gen-Air Study (EPIC Cohort).Nutrients · 2022Article
- Oxidative Stress and Antioxidative Therapy in Pulmonary Arterial Hypertension.Molecules (Basel, Switzerland) · 2022Review
- DNA-Protein Cross-Linking Sequencing for Genome-Wide Mapping of Thymidine Glycol.Journal of the American Chemical Society · 2022Article
- Site-Specific Synthesis of Oligonucleotides Containing 6-Oxo-MChemical research in toxicology · 2021Article
- Genome-wide mapping of genomic DNA damage: methods and implications.Cellular and molecular life sciences : CMLS · 2021Review
- Biomarkers of nucleic acid oxidation - A summary state-of-the-art.Redox biology · 2021Article
- Oxidative stress induction in woodworkers occupationally exposed to wood dust and formaldehyde.Journal of occupational medicine and toxicology (London, England) · 2021Article
- The Advanced Lipoxidation End-Product Malondialdehyde-Lysine in Aging and Longevity.Antioxidants (Basel, Switzerland) · 2020Review
- Mitochondrial DNA Damage: Prevalence, Biological Consequence, and Emerging Pathways.Chemical research in toxicology · 2020Review
- The hallmarks of severe pulmonary arterial hypertension: the cancer hypothesis-ten years later.American journal of physiology. Lung cellular and molecular physiology · 2020Review
- Genome-Wide Adductomics Analysis Reveals Heterogeneity in the Induction and Loss of Cyclobutane Thymine Dimers across Both the Nuclear and Mitochondrial Genomes.International journal of molecular sciences · 2019Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Reactive oxygen species (ROS) are formed in mitochondria during electron transport and energy generation. Elevated levels of ROS lead to increased amounts of mitochondrial DNA (mtDNA) damage. We report that levels of M1dG, a major endogenous peroxidation-derived DNA adduct, are 50-100-fold higher in mtDNA than in nuclear DNA in several different human cell lines. Treatment of cells with agents that either increase or decrease mitochondrial superoxide levels leads to increased or decreased levels of M1dG in mtDNA, respectively. Sequence analysis of adducted mtDNA suggests that M1dG residues are randomly distributed throughout the mitochondrial genome. Basal levels of M1dG in mtDNA from pulmonary microvascular endothelial cells (PMVECs) from transgenic bone morphogenetic protein receptor 2 mutant mice (BMPR2R899X) (four adducts per 106 dG) are twice as high as adduct levels in wild-type cells. A similar increase was observed in mtDNA from heterozygous null (BMPR2+/-) compared to wild-type PMVECs. Pulmonary arterial hypertension is observed in the presence of BMPR2 signaling disruptions, which are also associated with mitochondrial dysfunction and oxidant injury to endothelial tissue. Persistence of M1dG adducts in mtDNA could have implications for mutagenesis and mitochondrial gene expression, thereby contributing to the role of mitochondrial dysfunction in diseases.
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