ArticleFrontiers in neuroenergetics2013
Natural selection of mitochondria during somatic lifetime promotes healthy aging.
Article in Frontiers in neuroenergetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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.
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Who cites it
10 citing papers in PubMed, 19 citations in OpenAlex.
- Ketogenic diet for human diseases: the underlying mechanisms and potential for clinical implementations.Signal transduction and targeted therapy · 2022Review
- Maternal Protein Restriction in Two Successive Generations Impairs Mitochondrial Electron Coupling in the Progeny's Brainstem ofFrontiers in neuroscience · 2019Article
- ROS-Induced DNA Damage Associates with Abundance of Mitochondrial DNA in White Blood Cells of the Untreated Schizophrenic Patients.Oxidative medicine and cellular longevity · 2018Article
- Resistance training to improve type 2 diabetes: working toward a prescription for the future.Nutrition & metabolism · 2017Review
- A ketogenic diet accelerates neurodegeneration in mice with induced mitochondrial DNA toxicity in the forebrain.Neurobiology of aging · 2016Article
- Biology and Metabolism of Sepsis: Innate Immunity, Bioenergetics, and Autophagy.Surgical infections · 2016Review
- Article
- Redox signalling and mitochondrial stress responses; lessons from inborn errors of metabolism.Journal of inherited metabolic disease · 2015Review
- What is the function of mitochondrial networks? A theoretical assessment of hypotheses and proposal for future research.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015Review
- 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
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Stimulation of mitochondrial biogenesis during life-time challenges both eliminates disadvantageous properties and drives adaptive selection of advantageous phenotypic variations. Intermittent fission and fusion of mitochondria provide specific targets for health promotion by brief temporal stressors, interspersed with periods of recovery and biogenesis. For mitochondria, the mechanisms of selection, variability, and heritability, are complicated by interaction of two independent genomes, including the multiple copies of DNA in each mitochondrion, as well as the shared nuclear genome of each cell. The mechanisms of stress-induced fission, followed by recovery-induced fusion and biogenesis, drive the improvement of mitochondrial functions, not only as directed by genotypic variations, but also as enabled by phenotypic diversity. Selective adaptation may explain unresolved aspects of aging, including the health effects of exercise, hypoxic and poisonous preconditioning, and tissue-specific mitochondrial differences. We propose that intermittent purposeful enhancement of mitochondrial biogenesis by stressful episodes with subsequent recovery paradoxically promotes adaptive mitochondrial health and continued healthy aging.
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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.