ArticleNature2015
Exit from dormancy provokes DNA-damage-induced attrition in haematopoietic stem cells.
Article in Nature, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 391 papers, 1 of them a synthesis that pooled it.
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.
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.
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Who cites it
391 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Effects of fine particulate matter on bone marrow-conserved hematopoietic and mesenchymal stem cells: a systematic review.Experimental & molecular medicine · 2024Pooled it
- Severe hematopoietic stem cell inflammation compromises chronic granulomatous disease gene therapy.Cell reports. Medicine · 2023Trial
- Review
- Histone H3.3 ensures cell proliferation and genomic stability during myeloid cell development.iScience · 2026Article
- Activating an interleukin 4-FLT3-STAT6 axis in multipotent progenitors restores lymphopoiesis in inflammation and aging.Immunity · 2026Article
- Quantitative molecular cartography of emergency myelopoiesis reveals conserved modules of hematopoietic activation.Cell stem cell · 2026Article
- Should Sickle Cell Disease Be Considered a Cancer Predisposition Syndrome?Children (Basel, Switzerland) · 2026Review
- Lipid metabolism transcriptomic signature of defective erythropoiesis in Diamond Blackfan anemia syndrome.Blood advances · 2026Article
- Non-necroptotic MLKL function damages mitochondria and promotes hematopoietic stem cell aging.Nature communications · 2026Article
- Repeated proliferative events ameliorate age-associated accumulation of DNA damage in HSPCs.Life science alliance · 2026Article
- Unraveling the role ofHemaSphere · 2026Review
- Elevated endocytic trafficking mediated by GPRASP2 maintains HSC fidelity.bioRxiv : the preprint server for biology · 2026Article
- Fancl-mutant mice reveal central role of monoubiquitination in Fanconi anemia and a model for therapeutic gene editing.Blood advances · 2026Article
- Mutant p53 promotes clonal hematopoiesis by generating a chronic inflammatory microenvironment.The Journal of clinical investigation · 2026Article
- Molecular and phenotypic blueprint of human hematopoiesis links proliferation stress to stem cell aging.The Journal of experimental medicine · 2026Article
- Conserved stromal EMT program controls regenerative capacity of mesenchymal stromal cells across multiple tissues.Science advances · 2026Article
- The tight bond between Fanconi anemia and aging.Frontiers in aging · 2026Review
- Thrombopoietin increases susceptibility for EVI1 + KMT2A-MLLT3-driven AML expressing stem cell genes linked to poor outcome.Nature communications · 2025Article
- When Blood Disorders Meet Cancer: Uncovering the Oncogenic Landscape of Sickle Cell Disease.Journal of clinical medicine · 2025Review
- Metabolic adaptation of regenerative hematopoiesis depends on docking-independent mitochondrial connexin 43.Blood · 2025Article
331 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Haematopoietic stem cells (HSCs) are responsible for the lifelong production of blood cells. The accumulation of DNA damage in HSCs is a hallmark of ageing and is probably a major contributing factor in age-related tissue degeneration and malignant transformation. A number of accelerated ageing syndromes are associated with defective DNA repair and genomic instability, including the most common inherited bone marrow failure syndrome, Fanconi anaemia. However, the physiological source of DNA damage in HSCs from both normal and diseased individuals remains unclear. Here we show in mice that DNA damage is a direct consequence of inducing HSCs to exit their homeostatic quiescent state in response to conditions that model physiological stress, such as infection or chronic blood loss. Repeated activation of HSCs out of their dormant state provoked the attrition of normal HSCs and, in the case of mice with a non-functional Fanconi anaemia DNA repair pathway, led to a complete collapse of the haematopoietic system, which phenocopied the highly penetrant bone marrow failure seen in Fanconi anaemia patients. Our findings establish a novel link between physiological stress and DNA damage in normal HSCs and provide a mechanistic explanation for the universal accumulation of DNA damage in HSCs during ageing and the accelerated failure of the haematopoietic system in Fanconi anaemia patients.
Indexed as
Identifiers
25707806What 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.