ReviewMechanisms of ageing and development
Antagonistic pleiotropy and p53.
Review in Mechanisms of ageing and development. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Genetic Variants Associated With Resilience in Human and Animal Studies.Frontiers in psychiatry · 2022Pooled it
- Emerging New Pathways in Malignant Neoplasms and Neurodegenerative Disorders: Perspectives for Therapeutics.Cells · 2026Review
- Conserved Pathways, Divergent Outcomes: A Cross-Species Genomic Perspective on the Cancer-Neurodegeneration Paradox.International journal of molecular sciences · 2026Review
- Evolutionary perspectives on endometrial cancer: antagonistic pleiotropy.Molecular & cellular oncology · 2026Review
- Targeting immunosenesence promotes clearance of senescent cells.Immunity & ageing : I & A · 2025Review
- Phenotypic heterogeneity in human genetic diseases: ultrasensitivity-mediated threshold effects as a unifying molecular mechanism.Journal of biomedical science · 2023Review
- Selenoproteins and the senescence-associated epitranscriptome.Experimental biology and medicine (Maywood, N.J.) · 2022Review
- miR-71 mediates age-dependent opposing contributions of the stress-activated kinase KGB-1 in Caenorhabditis elegans.Genetics · 2021Article
- Human-specific polymorphic pseudogenization ofFASEB bioAdvances · 2021Article
- How can aging be reversed? Exploring rejuvenation from a damage-based perspective.Advanced genetics (Hoboken, N.J.) · 2020Article
- Review
- The endoplasmic reticulum acetyltransferases ATase1/NAT8B and ATase2/NAT8 are differentially regulated to adjust engagement of the secretory pathway.Journal of neurochemistry · 2020Article
- Review
- In Vitro Fertilization Technology and Child Health.Deutsches Arzteblatt international · 2020Review
- Contrasting Patterns of Rapid Molecular Evolution within the p53 Network across Mammal and Sauropsid Lineages.Genome biology and evolution · 2019Article
- How is the evolution of tumour resistance at organ-scale impacted by the importance of the organ for fitness?BMC evolutionary biology · 2018Article
- A Tale of Two Concepts: Harmonizing the Free Radical and Antagonistic Pleiotropy Theories of Aging.Antioxidants & redox signaling · 2018Review
- Possible Role of the Polyglutamine Elongation in Evolution of Amyloid-Related Evolvability.Journal of Huntington's disease · 2018Article
- Cancer and Aging - the Inflammatory Connection.Aging and disease · 2017Review
- miR-34a promotes fibrosis in aged lungs by inducing alveolarepithelial dysfunctions.American journal of physiology. Lung cellular and molecular physiology · 2017Article
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 1 institution in 1 country.
Funding
Abstract
George Williams' antagonistic pleiotropy theory of aging proposes that cellular damage and organismal aging are caused by pleiotrophic genes, or genes with multiple phenotypic effects [Williams, G.C., 1957. Pleiotropy, natural selection, and the evolution of senescence. Evolution 11, 398-411]. According to this theory, genes that exhibit antagonistic pleiotropy increase the odds of successful reproduction early in life, but have deleterious effects later in life. The tumor suppressor p53 confers protection against cancer (and death) by interrupting the abnormal proliferation of cells. When control of proliferation is applied to normal stem cells, however, it can impair tissue homeostasis and accelerate aging. We use data from recently developed models of accelerated aging in mice to determine if the deleterious effects of p53 on aging reflect antagonistic pleiotropy of the p53 gene or are attributable to genes that can modify p53 activity but are evolving independently.
Indexed as
Identifiers
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.