ReviewJournal of internal medicine2013
The role of mitochondrial DNA mutations and free radicals in disease and ageing.
Review in Journal of internal medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 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
126 citing papers in PubMed, 1 synthesis or guideline pooled it, 260 citations in OpenAlex.
- Comparative Analysis of the Complete Mitochondrial Genomes for Development Application.Frontiers in genetics · 2018Pooled it
- Structural and single-molecule insights into the core human mitochondrial DNA replisome.The Biochemical journal · 2026Review
- Nanomedicine-powered redox homeostasis modulation: Disrupting antioxidant systems and inducing oxidative stress for precision tumor therapy.Materials today. Bio · 2026Review
- Mitochondrial cardiovascular diseases: molecular mechanisms, multi-omics exploration and therapeutic strategies.Journal of advanced research · 2026Review
- Lifespan Predicts Mitochondrial Substitution Rates across Vertebrates, but Methodology Matters.Genome biology and evolution · 2026Article
- Aging at the Crossroads of Cuproptosis and Ferroptosis: From Molecular Pathways to Age-Related Pathologies and Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- The aging male: impact of aging on male reproduction.Biogerontology · 2025Review
- Non-pharmacological therapeutic paradigms in stress-induced depression: from novel therapeutic perspective with focus on cell-based strategies.Acta neuropsychiatrica · 2025Review
- Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial DNA Damage and Its Repair Mechanisms in Aging Oocytes.International journal of molecular sciences · 2024Review
- Modulating Mitochondrial DNA Heteroplasmy with Mitochondrially Targeted Endonucleases.Annals of biomedical engineering · 2024Review
- [A biobehavioral theoretical framework based on the mechanism of cellular aging for nursing interventions to promote autonomic balance].Journal of Korean biological nursing science · 2024Review
- Extracellular Delivery of Functional Mitochondria Rescues the Dysfunction of CD4Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- New insights into methods to measure biological age: a literature review.Frontiers in aging · 2024Review
- Zbp1 gene: a modulator of multiple aging hallmarks as potential therapeutic target for age-related diseases.Biogerontology · 2023Review
- Exploring the Role of Mediterranean and Westernized Diets and Their Main Nutrients in the Modulation of Oxidative Stress in the Placenta: A Narrative Review.Antioxidants (Basel, Switzerland) · 2023Review
- Modeling and Insights into the Structural Characteristics of Chemical Mitochondrial Toxicity.ACS omega · 2023Article
- Causal association between basal metabolic rate and risk of cardiovascular diseases: a univariable and multivariable Mendelian randomization study.Scientific reports · 2023Article
- Review
- Mitochondrial dysfunction: roles in skeletal muscle atrophy.Journal of translational medicine · 2023Review
66 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Considerable efforts have been made to understand the role of oxidative stress in age-related diseases and ageing. The mitochondrial free radical theory of ageing, which proposes that damage to mitochondrial DNA (mtDNA) and other macromolecules caused by the production of reactive oxygen species (ROS) during cellular respiration drives ageing, has for a long time been the central hypothesis in the field. However, in contrast with this theory, evidence from an increasing number of experimental studies has suggested that mtDNA mutations may be generated by replication errors rather than by accumulated oxidative damage. Furthermore, interventions to modulate ROS levels in humans and animal models have not produced consistent results in terms of delaying disease progression and extending lifespan. A number of recent experimental findings strongly question the mitochondrial free radical theory of ageing, leading to the emergence of new theories of how age-associated mitochondrial dysfunction may lead to ageing. These new hypotheses are mainly based on the underlying notion that, despite their deleterious role, ROS are essential signalling molecules that mediate stress responses in general and the stress response to age-dependent damage in particular. This novel view of ROS roles has a clear impact on the interpretation of studies in which antioxidants have been used to treat human age-related diseases commonly linked to oxidative stress.
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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.