ReviewAntioxidants & redox signaling2013
Alternative Perspectives on Aging in Caenorhabditis elegans: Reactive Oxygen Species or Hyperfunction?
Review in Antioxidants & redox signaling, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 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
121 citing papers in PubMed, 1 synthesis or guideline pooled it, 171 citations in OpenAlex.
- Pooled it
- Evolutionary genetics of ageing.Nature reviews. Genetics · 2026Review
- Adulthood depletion of Integrator extends lifespan and healthspan via defective pre-mRNA processing.bioRxiv : the preprint server for biology · 2026Article
- Review
- Machine learning predicts lifespan and suggests underlying causes of death in aging C. elegans.Communications biology · 2025Article
- A hierarchy of causes of death in senescentbioRxiv : the preprint server for biology · 2025Article
- Condition-dependent effects of knockdown of autophagy onbioRxiv : the preprint server for biology · 2025Article
- Review
- Epigenetic clocks and programmatic aging.Ageing research reviews · 2024Review
- Biological constraint, evolutionary spandrels and antagonistic pleiotropy.Ageing research reviews · 2024Review
- A unified framework for evolutionary genetic and physiological theories of aging.PLoS biology · 2024Article
- C. elegans ageing is accelerated by a self-destructive reproductive programme.Nature communications · 2023Article
- Towards disease-oriented dosing of rapamycin for longevity: does aging exist or only age-related diseases?Aging · 2023Article
- Article
- Article
- Endocytic coelomocytes are required for lifespan extension by axenic dietary restriction.PloS one · 2023Article
- Resolving Geroplasticity to the Balance of Rejuvenins and Geriatrins.Aging and disease · 2022Article
- Rapamycin treatment early in life reprograms aging: hyperfunction theory and clinical practice.Aging · 2022Article
- Axenic Culture ofInternational journal of molecular sciences · 2022Article
- Cell senescence, rapamycin and hyperfunction theory of aging.Cell cycle (Georgetown, Tex.) · 2022Review
61 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 1 institution in 1 country.
Funding
Abstract
significanceThe biological mechanisms at the heart of the aging process are a long-standing mystery. An influential theory has it that aging is the result of an accumulation of molecular damage, caused in particular by reactive oxygen species produced by mitochondria. This theory also predicts that processes that protect against oxidative damage (involving detoxification, repair, and turnover) protect against aging and increase lifespan. RECENT ADVANCES: However, recent tests of the oxidative damage theory, many using the short-lived nematode worm Caenorhabditis elegans, have often failed to support the theory. This motivates consideration of alternative models. One new theory, conceived by M.V. Blagosklonny, proposes that aging is caused by hyperfunction, that is, overactivity during adulthood of processes (particularly biosynthetic) that contribute to development and reproduction. Such hyperfunction can lead to hypertrophy-associated pathologies, which cause the age increase in death. CRITICAL ISSUES: Here we assess whether the hyperfunction theory is at all consistent with what is known about C. elegans aging, and conclude that it is. In particular, during adulthood, C. elegans shows a number of changes that may reflect pathology and/or hyperfunction. Such changes seem to contribute to death, at least in some cases (e.g., yolk accumulation). FUTURE DIRECTIONS: Our assessment suggests that the hyperfunction theory is a plausible alternative to the molecular damage theory to explain aging in C. elegans.
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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.