ReviewGenes2018
Is There Still Any Role for Oxidative Stress in Mitochondrial DNA-Dependent Aging?
Review in Genes, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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
40 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Oxidative Stress and Non-Alcoholic Fatty Liver Disease: Effects of Omega-3 Fatty Acid Supplementation.Nutrients · 2019Pooled it
- Low frequency mitochondrial DNA heteroplasmy SNPs in blood, retina, and [RPE+choroid] of age-related macular degeneration subjects.PloS one · 2021Trial
- Move beyond free radical theory of aging.iMetaOmics · 2026Review
- Ligase 3 prevents oxidative strand break-induced mitochondrial DNA loss but is not essential for replicative circularization.Nucleic acids research · 2025Article
- Interplay Between Aging and Glial Cell Dysfunction: Implications for CNS Health.Life (Basel, Switzerland) · 2025Review
- Article
- Whole Mitochondrial DNA Sequencing Using Fecal Samples from Domestic Dogs.Animals : an open access journal from MDPI · 2024Article
- Review
- Mitochondrial complex I deficiency stratifies idiopathic Parkinson's disease.Nature communications · 2024Article
- Association of Inflammatory Mediators with Mitochondrial DNA Variants in Geriatric COVID-19 Patients.Aging and disease · 2024Article
- Extracellular Delivery of Functional Mitochondria Rescues the Dysfunction of CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Review
- The Fate of Oxidative Strand Breaks in Mitochondrial DNA.Antioxidants (Basel, Switzerland) · 2023Article
- Targeting Mitochondria as a Therapeutic Approach for Parkinson's Disease.Cellular and molecular neurobiology · 2023Review
- A mitochondria-specific mutational signature of aging: increased rate of A > G substitutions on the heavy strand.Nucleic acids research · 2022Article
- Premature aging is associated with higher levels of 8-oxoguanine and increased DNA damage in the Polg mutator mouse.Aging cell · 2022Article
- Review
- The Mitochondrial Genome in Aging and Disease and the Future of Mitochondrial Therapeutics.Biomedicines · 2022Review
- Membrane lipids and maximum lifespan in clownfish.Fish physiology and biochemistry · 2022Article
- Mitochondrial Respiratory Chain Dysfunction-A Hallmark Pathology of Idiopathic Parkinson's Disease?Frontiers in cell and developmental biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent deep sequencing data has provided compelling evidence that the spectrum of somatic point mutations in mitochondrial DNA (mtDNA) in aging tissues lacks G > T transversion mutations. This fact cannot, however, be used as an argument for the missing contribution of reactive oxygen species (ROS) to mitochondria-related aging because it is probably caused by the nucleotide selectivity of mitochondrial DNA polymerase γ (POLG). In contrast to point mutations, the age-dependent accumulation of mitochondrial DNA deletions is, in light of recent experimental data, still explainable by the segregation of mutant molecules generated by the direct mutagenic effects of ROS (in particular, of HO· radicals formed from H₂O₂ by a Fenton reaction). The source of ROS remains controversial, because the mitochondrial contribution to tissue ROS production is probably lower than previously thought. Importantly, in the discussion about the potential role of oxidative stress in mitochondria-dependent aging, ROS generated by inflammation-linked processes and the distribution of free iron also require careful consideration.
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.