ReviewBioEssays : news and reviews in molecular, cellular and developmental biology2012
On the cause of aging and control of lifespan: heterogeneity leads to inevitable damage accumulation, causing aging; control of damage composition and rate of accumulation define lifespan.
Review in BioEssays : news and reviews in molecular, cellular and developmental biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 49 citations in OpenAlex.
- Foundations of Gerophysics.Aging · 2026Article
- Review
- Aging as the wound that fails to heal: a bioenergetic continuum of resolution failure.Biogerontology · 2025Review
- The Bioelectrics of Immortality and Mortality in Cold-SensitiveBioelectricity · 2025Article
- Multiomics reveals glutathione metabolism as a driver of bimodality during stem cell aging.Cell metabolism · 2023Article
- Approaches for completing metabolic networks through metabolite damage and repair discovery.Current opinion in systems biology · 2021Review
- The San Diego Nathan Shock Center: tackling the heterogeneity of aging.GeroScience · 2021Article
- Cellular aging beyond cellular senescence: Markers of senescence prior to cell cycle arrest in vitro and in vivo.Aging cell · 2021Review
- Age-dependent accumulation of dicarbonyls and advanced glycation endproducts (AGEs) associates with mitochondrial stress.Free radical biology & medicine · 2021Article
- The intrinsic apoptotic pathway lies upstream of oxidative stress in multiple organs.Free radical biology & medicine · 2020Article
- Microbial ageing and longevity.Nature reviews. Microbiology · 2019Review
- Telomere maintenance during anterior regeneration and aging in the freshwater annelid Aeolosoma viride.Scientific reports · 2018Article
- Protein synthesis and quality control in aging.Aging · 2018Review
- A Tale of Two Concepts: Harmonizing the Free Radical and Antagonistic Pleiotropy Theories of Aging.Antioxidants & redox signaling · 2018Review
- The role of glycation in the pathogenesis of aging and its prevention through herbal products and physical exercise.Journal of exercise nutrition & biochemistry · 2017Article
- Aging: progressive decline in fitness due to the rising deleteriome adjusted by genetic, environmental, and stochastic processes.Aging cell · 2016Review
- Tissue repair in myxobacteria: A cooperative strategy to heal cellular damage.BioEssays : news and reviews in molecular, cellular and developmental biology · 2016Article
- Which Is the Most Significant Cause of Aging?Antioxidants (Basel, Switzerland) · 2015Review
- Lazarillo-related Lipocalins confer long-term protection against type I Spinocerebellar Ataxia degeneration contributing to optimize selective autophagy.Molecular neurodegeneration · 2015Article
- The free radical theory of aging is dead. Long live the damage theory!Antioxidants & redox signaling · 2014Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
What the causes of aging are and which factors define lifespan are key questions in the understanding of aging. Here, it is argued that cellular life involves (i) inevitable accumulation of damage resulting from imperfectness and heterogeneity of every cellular process, and (ii) dilution of damage when cells divide. While severe damage is cleared by protective systems, milder damage can only be diluted. This is due to the high cost of accuracy, the greater number of damage forms compared to protective systems, and the constraints on cellular life inherited from the prokaryotic world. This strategy also applies to cancer cells, which are particularly dependent on damage dilution. Imposing restriction on cell division necessarily leads to aging. Interventions that extend lifespan act through metabolic reprogramming, thereby changing both damage composition and the rate of damage accumulation. Thus, heterogeneity leading to myriad mild damage forms represents the cause of aging, whereas the processes that affect the damage landscape and damage accumulation are lifespan regulators.
Indexed as
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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.