ReviewAgeing research reviews2024
Epigenetic clocks and programmatic aging.
Review in Ageing research reviews, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 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
32 citing papers in PubMed.
- Evolutionary genetics of ageing.Nature reviews. Genetics · 2026Review
- Extracellular vesicles and epigenetic aging clocks in tissue aging: an exosome-focused conceptual framework with a focus on skin.The journals of gerontology. Series A, Biological sciences and medical sciences · 2026Review
- The distinctiveness of human aging I: Anthropological and developmental foundations.Zeitschrift fur Gerontologie und Geriatrie · 2026Review
- Review
- Epigenetic clocks as quantitative readouts of epigenetic drift.Nature aging · 2026Article
- Systemic epigenetic dysregulation as a driver of ageing and a therapeutic target.Nature reviews. Molecular cell biology · 2026Review
- Epigenetic entropy, socioeconomic differences, and health and lifespan in the Women's Health Initiative.Clinical epigenetics · 2026Article
- The gut microbiome and ageing trajectories: mechanisms and clinical implications.Nature reviews. Endocrinology · 2026Review
- Multidimensional modeling of biological aging: integrating gait, eye movement, rest-state functional connectivity, and plasma biomarkers in non-dementia older adults.The journal of prevention of Alzheimer's disease · 2026Article
- The Evolving Landscape of Clinical Aging Clocks: From Epigenetic to Multi-Omics Integration.Aging cell · 2026Review
- DNA hypermethylation of FGFR2 drives fibrosis in the aging kidney.Scientific reports · 2026Article
- Multitissue, multi-time point transcriptomic atlas of aging in mice and rats.Science advances · 2026Article
- Pan-Epigenetic Age Prediction in Mammals.Aging cell · 2026Article
- Genetically Proxied Biological Aging and Risk of Hypertrophic Scar/Keloid-Coded Phenotypes: An Exploratory Two-Sample Mendelian Randomization Study.Clinical, cosmetic and investigational dermatology · 2026Article
- Salivary DNA methylation and pubertal development in adolescents.Scientific reports · 2025Article
- Aging by the clock and yet without a program.Nature aging · 2025Review
- The Bioelectrics of Immortality and Mortality in Cold-SensitiveBioelectricity · 2025Article
- How to measure and model cardiovascular aging.Cardiovascular research · 2025Review
- Dying occurs as a defined molecular progression iniScience · 2025Article
- Red Blood Cells and Human Aging: Exploring Their Biomarker Potential.Diagnostics (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
The last decade has seen remarkable progress in the characterization of methylation clocks that can serve as indicators of biological age in humans and many other mammalian species. While the biological processes of aging that underlie these clocks have remained unclear, several clues have pointed to a link to developmental mechanisms. These include the presence in the vicinity of clock CpG sites of genes that specify development, including those of the Hox (homeobox) and polycomb classes. Here we discuss how recent advances in programmatic theories of aging provide a framework within which methylation clocks can be understood as part of a developmental process of aging. This includes how such clocks evolve, how developmental mechanisms cause aging, and how they give rise to late-life disease. The combination of ideas from evolutionary biology, biogerontology and developmental biology open a path to a new discipline, that of developmental gerontology (devo-gero). Drawing on the properties of methylation clocks, we offer several new hypotheses that exemplify devo-gero thinking. We suggest that polycomb controls a trade-off between earlier developmental fidelity and later developmental plasticity. We also propose the existence of an evolutionarily-conserved developmental sequence spanning ontogenesis, adult development and aging, that both constrains and determines the evolution of 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.