ReviewThe Journal of cell biology2011
Mitochondrial DNA mutations in disease and aging.
Review in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 147 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
147 citing papers in PubMed, 1 synthesis or guideline pooled it, 308 citations in OpenAlex.
- Variability of Clinical Phenotypes Caused by Isolated Defects of Mitochondrial ATP Synthase.Physiological research · 2024Pooled it
- Rethinking the origins and functions of adaptive immunity.Trends in immunology · 2026Review
- Mitochondrial proteomics reveals reductive metabolism dependent on glutamine in fibroblasts of idiopathic pulmonary fibrosis under hypoxia.Scientific reports · 2026Article
- Reactive oxygen species (ROS) in cancer: from redox signaling and metabolic plasticity to therapeutic vulnerabilities.Exploration of targeted anti-tumor therapy · 2026Review
- Immunosenescence modulates radiation-induced anti-tumor immunity: implications for personalized immuno-oncology.Frontiers in immunology · 2026Review
- Article
- Silencing mitochondrial gene expression in living cells.Science (New York, N.Y.) · 2025Article
- Role of Mitochondrial Dysfunctions in Neurodegenerative Disorders: Advances in Mitochondrial Biology.Molecular neurobiology · 2025Review
- Exploring the role of mitochondrial dysfunction and aging in COVID-19-Related neurological complications.Molecular biology reports · 2025Review
- Revisiting the Role of Mitochondrial DNA Mutations in Aging: Bridging Theoretical Expectations with Empirical Observations.Aging and disease · 2025Review
- Aging through the lens of mitochondrial DNA mutations and inheritance paradoxes.Biogerontology · 2024Review
- Real-time assessment of mitochondrial DNA heteroplasmy dynamics at the single-cell level.The EMBO journal · 2024Article
- Crocetin Delays Brain and Body Aging by Increasing Cellular Energy Levels in Aged C57BL/6J Mice.ACS pharmacology & translational science · 2024Article
- Review
- Mitochondrial Dysfunctions: Genetic and Cellular Implications Revealed by Various Model Organisms.Genes · 2024Review
- Modulating Mitochondrial DNA Heteroplasmy with Mitochondrially Targeted Endonucleases.Annals of biomedical engineering · 2024Review
- Medaka (Animals : an open access journal from MDPI · 2024Article
- Endonuclease G is dispensable for sperm mitochondrial DNA elimination during spermatogenesis in mice.Biology open · 2024Article
- Genomic Mosaicism of the Brain: Origin, Impact, and Utility.Neuroscience bulletin · 2024Review
- The Role of TOMM40 in Cardiovascular Mortality and Conduction Disorders: An Observational Study.Journal of clinical medicine · 2024Article
87 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 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The small mammalian mitochondrial DNA (mtDNA) is very gene dense and encodes factors critical for oxidative phosphorylation. Mutations of mtDNA cause a variety of human mitochondrial diseases and are also heavily implicated in age-associated disease and aging. There has been considerable progress in our understanding of the role for mtDNA mutations in human pathology during the last two decades, but important mechanisms in mitochondrial genetics remain to be explained at the molecular level. In addition, mounting evidence suggests that most mtDNA mutations may be generated by replication errors and not by accumulated damage.
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.