ReviewNature aging2025
Aging by the clock and yet without a program.
Review in Nature aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 7 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
7 citing papers in PubMed.
- Semaglutide slows epigenetic aging in a randomized trial of HIV-associated lipohypertrophy.Nature communications · 2026Trial
- Poorer Physical Function Is Associated With Elevated Spatial Entropy in the Aging Brain Network Landscape.Aging cell · 2026Article
- Entropy of Muscle Fiber Histology Predicts Mobility in Older Adults: The Study of Muscle, Mobility, and Aging.Aging cell · 2026Article
- Mechanistic redundancy and hierarchy of aging mechanisms: implications for strategies to extend healthspan and biomarker integration.Frontiers in aging · 2026Review
- A sex-adjusted 7-biomarker clinical aging clock for translational preventative medicine.Scientific reports · 2025Article
- Entropy and Human Aging.Aging cell · 2025Article
- A Residual Approach to Estimate Biological Age from Gompertz Modeling.medRxiv : the preprint server for health sciences · 2025Article
Corrections and comments
- Erratum issued
Authors and funding
3 authors.
Funding
Abstract
The mechanisms of aging are becoming increasingly well mapped; however, there remains ongoing debate about the ultimate and proximate causes of aging. The recent development of highly precise aging clocks led to a resurgence of arguments in support of a biological program of aging. However, the declining force of natural selection after the onset of reproduction means that cellular function could deteriorate without requiring a specific program. Here, we argue that aging clocks do not imply an intrinsic program but rather reflect the stochastic accumulation of molecular errors and damage. Damage accumulates due to insufficient maintenance and repair and contributes to system-wide entropy. In support of this, cross-species comparisons indicate that enhanced DNA repair capacity is a key determinant of exceptional longevity in mammals. By better understanding the nature of the stochasticity that governs the aging process, we will have a stronger mechanistic basis for developing geroprotective interventions to promote healthy aging in humans.
Indexed as
Identifiers
40968181What 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.