ArticleAntioxidants & redox signaling2011
The p53/p21(WAF/CIP) pathway mediates oxidative stress and senescence in dyskeratosis congenita cells with telomerase insufficiency.
Article in Antioxidants & redox signaling, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 43 citations in OpenAlex.
- Association of nutraceutical supplements with longer telomere length.International journal of molecular medicine · 2019Trial
- Hyperoxia promotes bronchopulmonary dysplasia via Noggin-mediated BMP4 antagonism and cellular senescence.Frontiers in physiology · 2026Article
- Loss of Ten1 in mice induces telomere shortening and models human dyskeratosis congenita.Science advances · 2025Article
- PseudoCell: A Multivalued Logical Regulatory Network to Investigate Premature Senescence Dynamics and Heterogeneity.Aging medicine (Milton (N.S.W)) · 2025Article
- CRISPR screen identifies CEBPB as contributor to dyskeratosis congenita fibroblast senescence via augmented inflammatory gene response.G3 (Bethesda, Md.) · 2023Article
- The Molecular and Genetic Mechanisms of Inherited Bone Marrow Failure Syndromes: The Role of Inflammatory Cytokines in Their Pathogenesis.Biomolecules · 2023Review
- Review
- Germline thymidylate synthase deficiency impacts nucleotide metabolism and causes dyskeratosis congenita.American journal of human genetics · 2022Article
- Mesenchymal Stem/Stromal Cell Senescence: Hallmarks, Mechanisms, and Combating Strategies.Stem cells translational medicine · 2022Review
- The role of oxidative stress in intervertebral disc cellular senescence.Frontiers in endocrinology · 2022Review
- Bradykinin Protects Human Endothelial Progenitor Cells from High-Glucose-Induced Senescence through B2 Receptor-Mediated Activation of the Akt/eNOS Signalling Pathway.Journal of diabetes research · 2021Article
- NAD-Linked Metabolism and Intervention in Short Telomere Syndromes and Murine Models of Telomere Dysfunction.Frontiers in aging · 2021Review
- Discovery of potent telomerase activators: Unfolding new therapeutic and anti-aging perspectives.Molecular medicine reports · 2019Article
- Identification of telomerase RNAs in species of the Yarrowia clade provides insights into the co-evolution of telomerase, telomeric repeats and telomere-binding proteins.Scientific reports · 2019Article
- Article
- Defenses against Pro-oxidant Forces - Maintenance of Cellular and Genomic Integrity and Longevity.Radiation research · 2018Review
- A delayed proinflammatory response of human preadipocytes to PCB126 is dependent on the aryl hydrocarbon receptor.Environmental science and pollution research international · 2018Article
- Acute telomerase components depletion triggers oxidative stress as an early event previous to telomeric shortening.Redox biology · 2018Article
- Pulmonary complications post hematopoietic stem cell transplant in dyskeratosis congenita: analysis of oxidative stress in lung fibroblasts.Bone marrow transplantation · 2017Article
- Robust DNA Damage Response and Elevated Reactive Oxygen Species in TINF2-Mutated Dyskeratosis Congenita Cells.PloS one · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Telomere attrition is a natural process that occurs due to inadequate telomere maintenance. Once at a critically short threshold, telomeres signal growth arrest, leading to senescence. Telomeres can be elongated by the enzyme telomerase, which adds de novo telomere repeats to the ends of chromosomes. Mutations in genes for telomere binding proteins or components of telomerase give rise to the premature aging disorder dyskeratosis congenita (DC), which is characterized by extremely short telomeres and an aging phenotype. The current study demonstrates that DC cells signal a DNA damage response through p53 and its downstream mediator, p21(WAF/CIP), which is accompanied by an elevation in steady-state levels of superoxide and percent glutathione disulfide, both indicators of oxidative stress. Poor proliferation of DC cells can be partially overcome by reducing O(2) tension from 21% to 4%. Further, restoring telomerase activity or inhibiting p53 or p21(WAF/CIP) significantly mitigated growth inhibition as well as caused a significant decrease in steady-state levels of superoxide. Our results support a model in which telomerase insufficiency in DC leads to p21(WAF/CIP) signaling, via p53, to cause increased steady-state levels of superoxide, metabolic oxidative stress, and senescence.
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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.