ArticleAging cell2011
Accelerated hematopoietic stem cell aging in a mouse model of dyskeratosis congenita responds to antioxidant treatment.
Article in Aging cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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
22 citing papers in PubMed, 44 citations in OpenAlex.
- Dyskerin dysfunction in cancer development: from telomere dysregulation to immune deficiency.American journal of cancer research · 2026Review
- Deciphering the pseudouridine nucleobase modification in human diseases: From molecular mechanisms to clinical perspectives.Clinical and translational medicine · 2025Review
- Clinical mutations in the TERT and TERC genes coding for telomerase components induced oxidative stress, DNA damage at telomeres and cell apoptosis besides decreased telomerase activity.Human molecular genetics · 2024Article
- Aging-induced pseudouridine synthase 10 impairs hematopoietic stem cells.Haematologica · 2023Article
- Emerging Evidence of the Significance of Thioredoxin-1 in Hematopoietic Stem Cell Aging.Antioxidants (Basel, Switzerland) · 2022Review
- Dynamic changes in RNA-protein interactions and RNA secondary structure in mammalian erythropoiesis.Life science alliance · 2021Article
- Aging through an epitranscriptomic lens.Nature aging · 2021Review
- Article
- Article
- Cell competition corrects noisy Wnt morphogen gradients to achieve robust patterning in the zebrafish embryo.Nature communications · 2019Article
- Exonic Variants in Aging-Related Genes Are Predictive of Phenotypic Aging Status.Frontiers in genetics · 2019Article
- Acute telomerase components depletion triggers oxidative stress as an early event previous to telomeric shortening.Redox biology · 2018Article
- Redox-dependent BMI1 activity drives in vivo adult cardiac progenitor cell differentiation.Cell death and differentiation · 2018Article
- Robust DNA Damage Response and Elevated Reactive Oxygen Species in TINF2-Mutated Dyskeratosis Congenita Cells.PloS one · 2016Article
- Article
- Article
- Article
- Telomere shortening and Alzheimer's disease.Neuromolecular medicine · 2013Review
- Cell autonomous and nonautonomous mechanisms drive hematopoietic stem/progenitor cell loss in the absence of DNA repair.Stem cells (Dayton, Ohio) · 2013Article
- Dyskerin localizes to the mitotic apparatus and is required for orderly mitosis in human cells.PloS one · 2013Article
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 at 1 institution in 1 country.
Funding
Abstract
Mutations in DKC1, encoding telomerase associated protein dyskerin, cause X-linked dyskeratosis congenita (DC), a bone marrow (BM) failure, and cancer susceptibility syndrome. Decreased accumulation of telomerase RNA resulting in excessive telomere shortening and premature cellular senescence is thought to be the primary cause of disease in X-linked DC. Affected tissues are those that require constant renewal by stem cell activity. We previously showed that in Dkc1(Δ15) mice, which contain a mutation that is a copy of a human mutation causing DC, mutant cells have a telomerase-dependent proliferative defect and increased accumulation of DNA damage in the first generation before the telomeres are short. We now demonstrate the presence of the growth defect in Dkc1(Δ15) mouse embryonic fibroblasts in vitro and show that accumulation of DNA damage and levels of reactive oxygen species increase with increasing population doublings. Treatment with the antioxidant, N-acetyl cysteine (NAC), partially rescued the growth disadvantage of mutant cells in vitro and in vivo. Competitive BM repopulation experiments showed that the Dkc1(Δ15) mutation is associated with a functional stem cell defect that becomes more severe with increasing age, consistent with accelerated senescence, a hallmark of DC hematopoiesis. This stem cell phenotype was partially corrected by NAC treatment. These results suggest that a pathogenic Dkc1 mutation accelerates stem cell aging, that increased oxidative stress might play a role in the pathogenesis of X-linked DC, and that some manifestations of DC may be prevented or delayed by antioxidant treatment.
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.