ArticleAging cell2018
Clonal expansion of mitochondrial DNA deletions is a private mechanism of aging in long-lived animals.
Article in Aging cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Hypoxic-inflammatory preconditioning endows BMSC-derived appoptotic extracellular vesicles with potent efficacy against IVDD via cell activation and mitochondrial homeostasis regulation.Journal of nanobiotechnology · 2026Article
- Algal and Fungal Antioxidants Alleviate Oxidative Stress-Induced Reproductive Defects.Food science & nutrition · 2025Review
- Cryptic mitochondrial DNA mutations coincide with mid-late life and are pathophysiologically informative in single cells across tissues and species.Nature communications · 2025Article
- Mitochondrial DNA Damage and Its Repair Mechanisms in Aging Oocytes.International journal of molecular sciences · 2024Review
- Mitochondrial Reactive Oxygen Species Dysregulation in Heart Failure with Preserved Ejection Fraction: A Fraction of the Whole.Antioxidants (Basel, Switzerland) · 2024Review
- Maintaining mitochondrial DNA copy number mitigates ROS-induced oocyte decline and female reproductive aging.Communications biology · 2024Article
- Biomarkers in Thyroid Cancer: Emerging Opportunities from Non-Coding RNAs and Mitochondrial Space.International journal of molecular sciences · 2024Review
- Friend turned foe: selfish behavior of a spontaneously arising mitochondrial deletion in an experimentally evolved Caenorhabditis elegans population.G3 (Bethesda, Md.) · 2024Article
- Cardiovascular aging: spotlight on mitochondria.American journal of physiology. Heart and circulatory physiology · 2024Review
- Senolytics and cell senescence: historical and evolutionary perspectives.Evolution, medicine, and public health · 2024Article
- Energy substrate metabolism and oxidative stress in metabolic cardiomyopathy.Journal of molecular medicine (Berlin, Germany) · 2022Review
- Downregulating Mitochondrial DNA Polymerase γ in the Muscle Stimulated Autophagy, Apoptosis, and Muscle Aging-Related Phenotypes inBiomolecules · 2022Article
- C. elegans monitor energy status via the AMPK pathway to trigger innate immune responses against bacterial pathogens.Communications biology · 2022Article
- Mitochondrial protein import determines lifespan through metabolic reprogramming and de novo serine biosynthesis.Nature communications · 2022Article
- Mitochondrial DNA Is a Vital Driving Force in Ischemia-Reperfusion Injury in Cardiovascular Diseases.Oxidative medicine and cellular longevity · 2022Review
- Diagnostic and Therapeutic Roles of Extracellular Vesicles in Aging-Related Diseases.Oxidative medicine and cellular longevity · 2022Review
- Thermodynamic analysis of DNA hybridization signatures near mitochondrial DNA deletion breakpoints.iScience · 2021Article
- mtDNA Heteroplasmy at the Core of Aging-Associated Heart Failure. An Integrative View of OXPHOS and Mitochondrial Life Cycle in Cardiac Mitochondrial Physiology.Frontiers in cell and developmental biology · 2021Review
- Systematic analysis of a mitochondrial disease-causing ND6 mutation in mitochondrial deficiency.Molecular genetics & genomic medicine · 2020Article
- The rise and rise of mitochondrial DNA mutations.Open biology · 2020Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Disruption of mitochondrial metabolism and loss of mitochondrial DNA (mtDNA) integrity are widely considered as evolutionarily conserved (public) mechanisms of aging (López-Otín et al., Cell, 153, 2013 and 1194). Human aging is associated with loss in skeletal muscle mass and function (Sarcopenia), contributing significantly to morbidity and mortality. Muscle aging is associated with loss of mtDNA integrity. In humans, clonally expanded mtDNA deletions colocalize with sites of fiber breakage and atrophy in skeletal muscle. mtDNA deletions may therefore play an important, possibly causal role in sarcopenia. The nematode Caenorhabditis elegans also exhibits age-dependent decline in mitochondrial function and a form of sarcopenia. However, it is unclear if mtDNA deletions play a role in C. elegans aging. Here, we report identification of 266 novel mtDNA deletions in aging nematodes. Analysis of the mtDNA mutation spectrum and quantification of mutation burden indicates that (a) mtDNA deletions in nematode are extremely rare, (b) there is no significant age-dependent increase in mtDNA deletions, and (c) there is little evidence for clonal expansion driving mtDNA deletion dynamics. Thus, mtDNA deletions are unlikely to drive the age-dependent functional decline commonly observed in C. elegans. Computational modeling of mtDNA dynamics in C. elegans indicates that the lifespan of short-lived animals such as C. elegans is likely too short to allow for significant clonal expansion of mtDNA deletions. Together, these findings suggest that clonal expansion of mtDNA deletions is likely a private mechanism of aging predominantly relevant in long-lived animals such as humans and rhesus monkey and possibly in rodents.
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