ReviewNature aging2023
The meaning of adaptation in aging: insights from cellular senescence, epigenetic clocks and stem cell alterations.
Review in Nature aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 45 citations in OpenAlex.
- Liver-specific phenotypic aging, behavior and genetic risks, and long-term liver-related outcomes.GeroScience · 2026Article
- A Microenvironment-Adaptive Scaffold Rejuvenates Peripheral Nerve Regeneration During Aging Via Dual Modulation of Ferroptotic Stimuli in Schwann Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- KDM6A/MMP-3 epigenetic axis governs macrophage senescence after spinal cord injury for mediating the regenerative niche to promote neurological repair.Journal of advanced research · 2026Article
- Geroprotective applications of oleuropein and hydroxytyrosol through the hallmarks of ageing.GeroScience · 2026Review
- Proteomic aging clocks in epidemiological studies: advances, applications and prospects.Nature aging · 2026Review
- Boron as a Molecular Architect of Host-Microbiome Symbiosis: Implications for Dysbiosis and Aging-Related Pathologies.Life (Basel, Switzerland) · 2026Review
- Senescent Mesenchymal Stromal Cells Differentially Alter Adipogenesis in Adipose Tissue, Skeletal Muscle, and Bone Marrow.Obesity (Silver Spring, Md.) · 2026Article
- Hematopoietic (stem) cells-The elixir of life?FEBS letters · 2026Review
- PRC2-Related Epigenetic Age Acceleration in Acute Myeloid Leukemia with DNMT3A and IDH2 Mutations.Advanced biology · 2026Article
- Investigating epigenetic biomarkers of age, sex, and disease in captive South African cheetahs (Acinonyx jubatus jubatus).PloS one · 2026Article
- Rejuvenating the aging gut by targeting senescence.Nature aging · 2026Article
- A State-of-the-Art Overview on (Epi)Genomics and Personalized Skin Rejuvenating Strategies.Pharmaceutics · 2025Review
- Nucleosome stability safeguards cell identity, stress resilience and healthy aging.Research square · 2025Article
- Spatiotemporal-adaptive nanotherapeutics promote post-injury regeneration in ageing through metabolic modulation.Nature nanotechnology · 2025Article
- CD4 T cells acquire Eomesodermin to modulate cellular senescence and aging.Nature aging · 2025Article
- Aging: the wound that never starts healing.Nature communications · 2025Review
- Nucleosome stability safeguards cell identity, stress resilience and healthy aging.bioRxiv : the preprint server for biology · 2025Article
- Cells of all trades - on the importance of spatial positioning of senescent cells in development, healing and aging.FEBS letters · 2025Review
- Bibliometric insights into the cell cycle, aging, and metabolism: from molecular mechanisms to clinical implications.Biogerontology · 2025Review
- Addressing osteoblast senescence: Molecular pathways and the frontier of anti-ageing treatments.Clinical and translational medicine · 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
2 authors at 2 institutions in 2 countries.
Funding
Abstract
With recent rapid progress in research on aging, there is increasing evidence that many features commonly considered to be mechanisms or drivers of aging in fact represent adaptations. Here, we examine several such features, including cellular senescence, epigenetic aging and stem cell alterations. We draw a distinction between the causes and consequences of aging and define short-term consequences as 'responses' and long-term ones as 'adaptations'. We also discuss 'damaging adaptations', which despite having beneficial effects in the short term, lead to exacerbation of the initial insult and acceleration of aging. Features commonly recognized as 'basic mechanisms of the aging process' are critically examined for the possibility of their adaptation-driven emergence from processes such as cell competition and the wound-like features of the aging body. Finally, we speculate on the meaning of these interactions for the aging process and their relevance for the development of antiaging interventions.
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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.