ReviewChinese medical journal2026
Epigenetic dynamics of cellular senescence: From mechanistic insights to precision senotherapy.
Review in Chinese medical journal, 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.
- Oncoviruses at the Crossroads of Ageing and Cancer: Molecular Mechanisms and Key Signalling Pathways.Reviews in medical virology · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
abstractCellular senescence functions as a pivotal stress response with dual roles; it serves as a barrier against early tumorigenesis while paradoxically driving late-stage tumor progression and the pathogenesis of many other age-related diseases, including cardiovascular, neurodegenerative, metabolic, and fibrotic disorders. This review comprehensively elucidates how the senescent phenotype is orchestrated by a dynamic epigenetic landscape. We detail how dysregulation in chromatin remodeling (e.g., heterochromatin loss), histone modifications, DNA methylation, and the epitranscriptome rewrites genome architecture to govern the initiation and maintenance of the senescent phenotype within these specific disease contexts. Crucially, we highlight the profound heterogeneity of senescence across different pathologies, contrasting its detrimental role in driving tissue degeneration in organs like the lung and kidney against its context-dependent beneficial effects, such as limiting fibrosis in the liver. Furthermore, we evaluate the translational potential of epigenetic drugs-categorized by targets such as DNA methyltransferases (DNMTs), histone methyltransferases (HMTs), and histone deacetylases (HDACs)-as dual-purpose therapeutics. Unlike genetic mutations, epigenetic alterations are reversible. We discuss strategies to either enforce senescence barriers for cancer suppression (pro-senescence) or reverse epigenetic aging signatures for tissue rejuvenation (anti-senescence). This review proposes a roadmap for leveraging epigenetic plasticity, offering a precision medicine approach to target specific senescent cell populations and extend health span.
Indexed as
Identifiers
What Socratic 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 Socratic graph.