ReviewAging and disease2013
mtDNA Mutations and Their Role in Aging, Diseases and Forensic Sciences.
Review in Aging and disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 68 citations in OpenAlex.
- Correlations between Aging, Telomeres, and Natural Compounds.Aging and disease · 2025Review
- Targeting the Electron Transport System for Enhanced Longevity.Biomolecules · 2025Review
- GDF15 Neutralization Ameliorates Muscle Atrophy and Exercise Intolerance in a Mouse Model of Mitochondrial Myopathy.Journal of cachexia, sarcopenia and muscle · 2025Article
- Effects of molecular interactions between the exposome and oxylipin metabolism on healthspan.Frontiers in physiology · 2025Review
- Connection Between HIV and Mitochondria in Cardiovascular Disease and Implications for Treatments.Circulation research · 2024Review
- Development of MitoWizz: a Bioinformatics Solution for Mitochondrial DNA Analysis in Both Forensic and Clinical Applications.Acta informatica medica : AIM : journal of the Society for Medical Informatics of Bosnia & Herzegovina : casopis Drustva za medicinsku informatiku BiH · 2024Article
- Cardiovascular aging: the mitochondrial influence.The journal of cardiovascular aging · 2023Article
- Breaking the vicious cycle: The interplay between loneliness, metabolic illness, and mental health.Frontiers in psychiatry · 2023Article
- Investigating the Impact of a Curse: Diseases, Population Isolation, Evolution and the Mother's Curse.Genes · 2022Review
- Role of Oxidative Stress and Antioxidants in Acquired Inner Ear Disorders.Antioxidants (Basel, Switzerland) · 2022Review
- Relationship between oxidative stress and lifespan in Daphnia pulex.Scientific reports · 2022Article
- Next-generation sequencing of the whole mitochondrial genome identifies novel and common variants in patients with psoriasis, type 2 diabetes mellitus and psoriasis with comorbid type 2 diabetes mellitus.Biomedical reports · 2021Article
- De Novo Development of mtDNA Deletion Due to Decreased POLG and SSBP1 Expression in Humans.Genes · 2021Article
- Mitochondrial DNA Depletion Syndrome and Its Associated Cardiac Disease.Frontiers in cardiovascular medicine · 2021Review
- Testosterone enhances mitochondrial complex V function in the substantia nigra of aged male rats.Aging · 2020Article
- Stem Cells of the Aging Brain.Frontiers in aging neuroscience · 2020Review
- Frailty, Cognitive Decline, Neurodegenerative Diseases and Nutrition Interventions.International journal of molecular sciences · 2019Review
- Variation in Mitochondria-Derived Transcript Levels Associated With DDT Resistance in the 91-R Strain of Drosophila melanogaster (Diptera: Drosophilidae).Journal of insect science (Online) · 2018Article
- Toxicity of nanotitanium dioxide (TiOEnvironmental science and pollution research international · 2018Article
- Exposure to Antineoplastic Agents Induces Cytotoxicity in Nurse Lymphocytes: Role of Mitochondrial Damage and Oxidative Stress.Iranian journal of pharmaceutical research : IJPR · 2018Article
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
Mitochondria are independent organelles with their own DNA. As a primary function, mitochondria produce the energy for the cell through Oxidative Phosphorylation (OXPHOS) in the Electron Transport Chain (ETC). One of the toxic products of this process is Reactive Oxygen Species (ROS), which can induce oxidative damage in macromolecules like lipids, proteins and DNA. Mitochondrial DNA (mtDNA) is less protected and has fewer reparation mechanisms than nuclear DNA (nDNA), and as such is more exposed to oxidative, mutation-inducing damage. This review analyzes the causes and consequences of mtDNA mutations and their relationship with the aging process. Neurodegenerative diseases, related with the aging, are consequences of mtDNA mutations resulting in a decrease in mitochondrial function. Also described are "mitochondrial diseases", pathologies produced by mtDNA mutations and whose symptoms are related with mitochondrial dysfunction. Finally, mtDNA haplogroups are defined in this review; these groups are important for determination of geographical origin of an individual. Additionally, different haplogroups exhibit variably longevity and risk of certain diseases. mtDNA mutations in aging and haplogroups are of special interest to forensic science research. Therefore this review will help to clarify the key role of mtDNA mutations in these processes and support further research in this area.
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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.