ReviewAging cell2016
Aging: progressive decline in fitness due to the rising deleteriome adjusted by genetic, environmental, and stochastic processes.
Review in Aging cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 131 papers, 2 of them syntheses 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
131 citing papers in PubMed, 2 syntheses or guidelines pooled it, 257 citations in OpenAlex.
- Social determinants of health and epigenetic clocks: a systematic review and meta-analysis of 140 studies.Nature human behaviour · 2026Pooled it
- Association between telomere length, frailty and death in older adults.GeroScience · 2021Pooled it
- Effects of photobiomodulation on muscle strength in post-menopausal women submitted to a resistance training program.Lasers in medical science · 2020Trial
- Protein thiol alterations drive pathologic liquid-liquid phase separation in the aging brain.Nature structural & molecular biology · 2026Article
- Systemic epigenetic dysregulation as a driver of ageing and a therapeutic target.Nature reviews. Molecular cell biology · 2026Review
- Mammalian aging involves genome-wide splicing degeneration leading to functional decline.bioRxiv : the preprint server for biology · 2026Article
- Article
- Foundations of Gerophysics.Aging · 2026Article
- Old worms, new tricks: dynamical instability explains late-life rejuvenation inbioRxiv : the preprint server for biology · 2026Article
- Article
- Glycative Stress Disrupts the Mitochondrial-Lysosome Axis and Promotes Geroconversion in Aging Cardiomyocytes.Aging cell · 2026Article
- Limitations of Daily Step Count for Assessing Health in Older Adults: The Need to Consider Walking Intensity.Epidemiologia (Basel, Switzerland) · 2026Article
- In Vivo Chemical Reprogramming Is Associated With a Toxic Accumulation of Lipid Droplets Hindering Rejuvenation.Aging cell · 2026Article
- Mitochondria as a Therapeutic Target in Neurodegeneration: Strategies for Restoring Cellular Homeostasis.Current neuropharmacology · 2026Review
- Rejuvenation of white adipose tissue in a longitudinal heterochronic transplantation model.bioRxiv : the preprint server for biology · 2025Article
- Association of biological age acceleration with mortality in adults with diabetes or prediabetes: a mediating role of physical activity.Aging clinical and experimental research · 2025Article
- Accelerated transcriptomic age and susceptibility to traffic-related air pollution among cardiac catheterization patients.The Science of the total environment · 2025Article
- The dissipation theory of aging: a quantitative analysis using a cellular aging map.npj aging · 2025Article
- Individual and Comorbid Influences of Chronic Stress and a Western Diet on Allostatic Loads and Cardiac Resilience, Adaptation and Proteome Profiles in Male Mice.Comprehensive Physiology · 2025Article
- The association of a polygenic lifespan score with the risk of common age-related diseases and mortality.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025Article
71 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
1 author at 1 institution in 1 country.
Funding
Abstract
Different theories posit that aging is caused by molecular damage, genetic programs, continued development, hyperfunction, antagonistic pleiotropy alleles, mutations, trade-offs, incomplete repair, etc. Here, I discuss that these ideas can be conceptually unified as they capture particular facets of aging, while being incomplete. Their respective deleterious effects impact fitness at different levels of biological organization, adjusting progression through aging, rather than causing it. Living is associated with a myriad of deleterious processes, both random and deterministic, which are caused by imperfectness, exhibit cumulative properties, and represent the indirect effects of biological functions at all levels, from simple molecules to systems. From this, I derive the deleteriome, which encompasses cumulative deleterious age-related changes and represents the biological age. The organismal deleteriome consists of the deleteriomes of cells, organs, and systems, which change along roughly synchronized trajectories and may be assessed through biomarkers of aging. Aging is then a progressive decline in fitness due to the increasing deleteriome, adjusted by genetic, environmental, and stochastic processes. This model allows integration of diverse aging concepts, provides insights into the nature of aging, and suggests how lifespan may be adjusted during evolution and in experimental models.
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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.