ReviewLife medicine2022
Aging-associated accumulation of mitochondrial DNA mutations in tumor origin.
Review in Life medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed.
- Mitochondria-Targeted Nanotherapies in Aging Neurodegenerative Disorders: Emerging Prospects and Clinical Potential.Advanced healthcare materials · 2026Review
- Mitophagy and Noncoding RNA Regulation in Type 2 Diabetes Mellitus: Molecular Mechanisms, Tissue-Specific Evidence and Translational Perspective.Biomedicines · 2026Review
- Targeting Mitochondria for Postoperative Cognitive Dysfunction: From Mechanisms to Therapeutics.Molecular neurobiology · 2026Review
- Internet Gaming Addiction in Male Adolescents: Mitochondrial DNA Variations and Leukocyte Telomere Length.Genes · 2026Article
- Cellular Senescence and Aging: Mechanisms, Disease Convergence, and Therapeutic Frontiers.MedComm · 2026Review
- Mitochondrial NADH-redox inflexibility constrains genomic and epigenetic stability in pluripotent stem cells.The EMBO journal · 2026Article
- Epigenetics, Oxidative Stress, and the Microbiome in Endometriosis: Toward an Integrated Mechanistic Framework for Precision Medicine.Journal of personalized medicine · 2026Review
- Redox-Regulated Mitophagy and Lysosomal Dysfunction as a Convergent Mechanism in Female Infertility: Molecular Insights and Therapeutic Perspectives.Current issues in molecular biology · 2026Review
- The cGAS-STING pathway at the crossroads of neuroimmunology: bridging innate immunity to aging and neurodegeneration.Biomarker research · 2026Review
- Mitochondrial DNA mutations and intercellular mitochondrial transfer in cancer: mechanisms, biological effects, and clinical potential.Biomarker research · 2026Review
- Article
- Mitochondrial sirtuins, key regulators of aging.Life medicine · 2025Review
- Impaired Mitochondrial DNA Copy Number in Visceral Adipose Tissue of Insulin-Resistant Individuals: Implications for Metabolic Dysregulation.International journal of molecular sciences · 2025Article
- Mitochondrial dysfunction in the regulation of aging and aging-related diseases.Cell communication and signaling : CCS · 2025Review
- scCancerExplorer: a comprehensive database for interactively exploring single-cell multi-omics data of human pan-cancer.Nucleic acids research · 2025Article
- Aging through the lens of mitochondrial DNA mutations and inheritance paradoxes.Biogerontology · 2024Review
- Facts, Dogmas, and Unknowns About Mitochondrial Reactive Oxygen Species in Cancer.Antioxidants (Basel, Switzerland) · 2024Review
- Single-cell mitochondrial sequencing reveals low-frequency mitochondrial mutations in naturally aging mice.Aging cell · 2024Article
- Antioxidants and Mechanistic Insights for Managing Dry Age-Related Macular Degeneration.Antioxidants (Basel, Switzerland) · 2024Review
- The Warburg effect drives dedifferentiation through epigenetic reprogramming.Cancer biology & medicine · 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
7 authors.
Funding
Abstract
The majority of cancer patients are among aged population, suggesting an urgent need to advance our knowledge on complicated relationship between aging and cancer. It has been hypothesized that metabolic changes during aging could act as a driver for tumorigenesis. Given the fact that mitochondrial DNA (mtDNA) mutations are common in both tumors and aged tissues, it is interesting to contemplate possible role of age-related mtDNA mutations in tumorigenesis. MtDNA encodes genes essential for mitochondrial metabolism, and mtDNA mutates at a much higher rate than nuclear genome. Random drifting of somatic mtDNA mutations, as a result of cell division or mitochondrial turnover during aging, may lead to more and more cells harboring high-frequency pathogenic mtDNA mutations, albeit at different loci, in single-cells. Such mutations can induce metabolic reprogramming, nuclear genome instability and immune response, which might increase the likelihood of tumorigenesis. In this review, we summarize current understanding of how mtDNA mutations accumulate with aging and how these mutations could mechanistically contribute to tumor origin. We also discuss potential prevention strategies for mtDNA mutation-induced tumorigenesis, and future works needed in this direction.
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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.