ArticleCell stem cell2014
Quiescent hematopoietic stem cells accumulate DNA damage during aging that is repaired upon entry into cell cycle.
Article in Cell stem cell, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 280 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
280 citing papers in PubMed, 1 synthesis or guideline pooled it, 432 citations in OpenAlex.
- Biological effects of cancer stem cells irradiated by charged particle: a systematic review of in vitro studies.Journal of cancer research and clinical oncology · 2023Pooled it
- Westernized diet related arachidonic acid metabolism expands DNA error-prone growth factor-dependent colonic quiescent stem cells in adolescent mice.Cell death & disease · 2026Article
- IDEAL-Age: an interpretable deep learning framework for single-cell resolution profiling of immunological aging.Genome biology · 2026Article
- Loss of tissue-state plasticity: a conceptual framework for age-associated regenerative failure.Inflammation and regeneration · 2026Review
- Epigenetic programming by H3K23ac defines lineage fate of Meg3Nature cell biology · 2026Article
- Aging mechanisms and rejuvenation strategies for hematopoietic stem cells.Genome biology · 2026Review
- Translational Geroscience Strategies for Delaying Multimorbidity.ACS pharmacology & translational science · 2026Review
- Age-Like Methylation Changes of HSCs in GADD45B Knockout Mice Define Methylation Sites Associated With Loss of Function.Aging cell · 2026Article
- Repeated proliferative events ameliorate age-associated accumulation of DNA damage in HSPCs.Life science alliance · 2026Article
- Article
- Molecular and phenotypic blueprint of human hematopoiesis links proliferation stress to stem cell aging.The Journal of experimental medicine · 2026Article
- Article
- Cholesterol sulfate replenishment rejuvenates aged hematopoietic stem cell phenomes.Theranostics · 2026Article
- From molecular damage to regulatory constraint: epigenetic and metabolic limits of cellular plasticity in aging.Frontiers in aging · 2026Review
- Lineage tracing of both quiescent G0 and active Hoxb5+ LT-HSCs that actively contribute to homeostatic mouse hematopoiesis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- DNA shape and epigenomics distinguish the mechanistic origin of human genomic structural variations.Nucleic acids research · 2025Article
- Article
- Proneural-mesenchymal hybrid glioblastoma cells are resistant to therapy and dependent on nuclear import.Neuro-oncology · 2025Article
- Hematopoietic Stem Cell Aging: Mechanisms, Microenvironment Influences, and Rejuvenation Strategies.Bioengineering (Basel, Switzerland) · 2025Review
- P-selectin overexpression impairs hematopoietic stem cell homeostasis via inflammatory receptor-mediated proliferation and differentiation.Cell death & disease · 2025Article
220 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Hematopoietic stem cells (HSCs) maintain homeostasis and regenerate the blood system throughout life. It has been postulated that HSCs may be uniquely capable of preserving their genomic integrity in order to ensure lifelong function. To directly test this, we quantified DNA damage in HSCs and downstream progenitors from young and old mice, revealing that strand breaks significantly accrue in HSCs during aging. DNA damage accumulation in HSCs was associated with broad attenuation of DNA repair and response pathways that was dependent upon HSC quiescence. Accordingly, cycling fetal HSCs and adult HSCs driven into cycle upregulated these pathways leading to repair of strand breaks. Our results demonstrate that HSCs are not comprehensively geno-protected during aging. Rather, HSC quiescence and concomitant attenuation of DNA repair and response pathways underlies DNA damage accumulation in HSCs during aging. These results provide a potential mechanism through which premalignant mutations accrue in HSCs.
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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.