ReviewBiogerontology2026
"Metabolic memory" of aging: anchoring, transmission, and frontiers of transgenerational intervention.
Review in Biogerontology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The metabolic-epigenetic landscape of aging: interplay between histone acetylation, lactylation, and glycation.Frontiers in aging · 2026Review
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cellular senescence is the core cytological basis for organismal aging and the development of age-related diseases. Accumulating evidence indicates that senescent phenotypes can be maintained long-term even after the removal of senescence-inducing stressors, and may even affect daughter cells and offspring. This review systematically proposes an integrated theoretical framework of "aging metabolic memory", explaining the persistence, transmissibility, and potential heritability of aging from a systems biology perspective. First, it elaborates on how mitochondrial metabolic reprogramming reshapes the cellular epigenetic landscape (DNA methylation, histone modification) by altering the homeodynamics of key metabolites (NAD⁺, α-ketoglutarate, succinate, etc.), thereby forming stable senescence imprints; second, it in-depth analyzes the mechanisms by which the senescence-associated secretory phenotype (SASP) and extracellular vesicles (EVs) act as "memory carriers" to achieve intercellular transmission and systemic spread of senescent phenotypes; on this basis, combined with the latest progress in epigenetics, it proposes and demonstrates a hypothetical model for the transgenerational transmission of aging metabolic memory through germ cells, exploring its biological significance and evolutionary implications; finally, it systematically sorts out and prospects novel aging intervention strategies based on "memory intervention" (rather than mere elimination), including metabolic resetting, epigenetic remodeling, transmission blocking, and germ cell-targeted intervention. This review summarizes the spatiotemporal dynamic characteristics of aging and may provide multi-dimensional intervention pathways for the precise prevention and treatment of age-related diseases and the promotion of healthy aging.
Indexed as
Identifiers
41721930What 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.