ArticleMechanisms of ageing and development2009
Altered senescence, apoptosis, and DNA damage response in a mutant p53 model of accelerated aging.
Article in Mechanisms of ageing and development, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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Who cites it
24 citing papers in PubMed, 45 citations in OpenAlex.
- Colonic inflammatory response in a D-galactose-induced aging model: elevated IL-1β expression.Journal of molecular histology · 2026Article
- Premature renal epithelial cell senescence promoted by LXN/Rps3/p53 signaling pathway activation increases calcium oxalate crystal deposition by altering macrophage polarization.Frontiers in immunology · 2025Article
- The cell cycle regulator p16 promotes tumor infiltrated CD8Cell death & disease · 2024Article
- Acetylation of Atp5f1c Mediates Cardiomyocyte Senescence via Metabolic Dysfunction in Radiation-Induced Heart Damage.Oxidative medicine and cellular longevity · 2022Article
- The Δ40p53 isoform inhibits p53-dependent eRNA transcription and enables regulation by signal-specific transcription factors during p53 activation.PLoS biology · 2021Article
- From DNA damage to mutations: All roads lead to aging.Ageing research reviews · 2021Review
- Oxidative Stress and Gene Expression Modifications Mediated by Extracellular Vesicles: An In Vivo Study of the Radiation-Induced Bystander Effect.Antioxidants (Basel, Switzerland) · 2021Article
- Iron accumulation in senescent cells is coupled with impaired ferritinophagy and inhibition of ferroptosis.Redox biology · 2018Article
- Haploinsufficiency ofeLife · 2018Article
- p53 and the Carcinogenicity of Chronic Inflammation.Cold Spring Harbor perspectives in medicine · 2016Review
- BRD4 Connects Enhancer Remodeling to Senescence Immune Surveillance.Cancer discovery · 2016Article
- Combined activation of the energy and cellular-defense pathways may explain the potent anti-senescence activity of methylene blue.Redox biology · 2015Article
- Metabolic regulation by p53 family members.Cell metabolism · 2013Review
- Postnatal development, maturation and aging in the mouse cochlea and their effects on hair cell regeneration.Hearing research · 2013Review
- Cdkn1b overexpression in adult mice alters the balance between genome and tissue ageing.Nature communications · 2013Article
- Impaired antioxidant defence and accumulation of oxidative stress in caspase-2-deficient mice.Cell death and differentiation · 2012Article
- The quiescent cellular state is Arf/p53-dependent and associated with H2AX downregulation and genome stability.International journal of molecular sciences · 2012Review
- Inflammation and p53: A Tale of Two Stresses.Genes & cancer · 2011Article
- Apoptosis and aging: increased resistance to apoptosis enhances the aging process.Cellular and molecular life sciences : CMLS · 2011Review
- Four faces of cellular senescence.The Journal of cell biology · 2011Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The tumor suppressors p16(INK4a) and p53 have been implicated as contributors to age-associated stem cell decline. Key functions of p53 are the induction of cell cycle arrest, senescence, or apoptosis in response to DNA damage. Here, we examine senescence, apoptosis, and DNA damage responses in a mouse accelerated aging model that exhibits increased p53 activity, the p53(+/m) mouse. Aged tissues of p53(+/m) mice display higher percentages of senescent cells (as determined by senescence-associated beta-galactosidase staining and p16(INK4a) and p21 accumulation) compared to aged tissues from p53(+/+) mice. Surprisingly, despite having enhanced p53 activity, p53(+/m) lymphoid tissues exhibit reduced apoptotic activity in response to ionizing radiation compared to p53(+/+) tissues. Ionizing radiation treatment of p53(+/m) tissues also induces higher and prolonged levels of senescence markers p16(INK4a) and p21, suggesting that in p53(+/m) tissues the p53 stress response is enhanced and is shifted away from apoptosis toward senescence. One potential mechanism for accelerated aging in the p53(+/m) mouse is a failure to remove damaged or dysfunctional cells (including stem and progenitor cells) through apoptosis. The increased accumulation of dysfunctional and senescent cells may contribute to reduced tissue regeneration, tissue atrophy, and some of the accelerated aging phenotypes in p53(+/m) mice.
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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.