ReviewAgeing research reviews2011
Mitochondrial-nuclear epistasis: implications for human aging and longevity.
Review in Ageing research reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 56 citations in OpenAlex.
- Meta-analysis identifies mitochondrial DNA sequence variants associated with walking speed.GeroScience · 2018Pooled it
- The role of mitotype variation and positive epistasis in trait differences between Saccharomyces species.Genetics · 2026Article
- The significance of mitochondrial DNA changes during the onset and progression of head and neck squamous cell carcinoma.Future oncology (London, England) · 2026Review
- Article
- Article
- Longevity, Centenarians and Modified Cellular Proteodynamics.International journal of molecular sciences · 2023Review
- Restoring fertility in yeast hybrids: Breeding and quantitative genetics of beneficial traits.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Intricacies of aetiology in intrafamilial degenerative disease.Brain communications · 2020Review
- Mitochondrial ROS-Modulated mtDNA: A Potential Target for Cardiac Aging.Oxidative medicine and cellular longevity · 2020Review
- Mito-nuclear interactions modify Drosophila exercise performance.Mitochondrion · 2019Article
- Nuclear-Mitochondrial interactions influence susceptibility to HIV-associated neurocognitive impairment.Mitochondrion · 2019Observational
- Mitochondria: multifaceted regulators of aging.BMB reports · 2019Review
- Mitochondrial DNA Sequence Variants Associated With Blood Pressure Among 2 Cohorts of Older Adults.Journal of the American Heart Association · 2018Article
- Mitochondrial DNA variation and the pathogenesis of osteoarthritis phenotypes.Nature reviews. Rheumatology · 2018Review
- Admixture Effects on Coevolved Metabolic Systems.Frontiers in genetics · 2018Article
- Candidate gene resequencing to identify rare, pedigree-specific variants influencing healthy aging phenotypes in the long life family study.BMC geriatrics · 2016Article
- Mitochondrial-nuclear epistasis contributes to phenotypic variation and coadaptation in natural isolates of Saccharomyces cerevisiae.Genetics · 2014Article
- Inherited mitochondrial DNA variants can affect complement, inflammation and apoptosis pathways: insights into mitochondrial-nuclear interactions.Human molecular genetics · 2014Article
- The emergence of the mitochondrial genome as a partial regulator of nuclear function is providing new insights into the genetic mechanisms underlying age-related complex disease.Human genetics · 2014Review
- The three genetics (nuclear DNA, mitochondrial DNA, and gut microbiome) of longevity in humans considered as metaorganisms.BioMed research international · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
There is substantial evidence that mitochondria are involved in the aging process. Mitochondrial function requires the coordinated expression of hundreds of nuclear genes and a few dozen mitochondrial genes, many of which have been associated with either extended or shortened life span. Impaired mitochondrial function resulting from mtDNA and nuclear DNA variation is likely to contribute to an imbalance in cellular energy homeostasis, increased vulnerability to oxidative stress, and an increased rate of cellular senescence and aging. The complex genetic architecture of mitochondria suggests that there may be an equally complex set of gene interactions (epistases) involving genetic variation in the nuclear and mitochondrial genomes. Results from Drosophila suggest that the effects of mtDNA haplotypes on longevity vary among different nuclear allelic backgrounds, which could account for the inconsistent associations that have been observed between mitochondrial DNA (mtDNA) haplogroups and survival in humans. A diversity of pathways may influence the way mitochondria and nuclear-mitochondrial interactions modulate longevity, including: oxidative phosphorylation; mitochondrial uncoupling; antioxidant defenses; mitochondrial fission and fusion; and sirtuin regulation of mitochondrial genes. We hypothesize that aging and longevity, as complex traits having a significant genetic component, are likely to be controlled by nuclear gene variants interacting with both inherited and somatic mtDNA variability.
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.