ArticleCell reports2015
Stem Cell-Specific Mechanisms Ensure Genomic Fidelity within HSCs and upon Aging of HSCs.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 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
34 citing papers in PubMed.
- Repeated proliferative events ameliorate age-associated accumulation of DNA damage in HSPCs.Life science alliance · 2026Article
- The systemic costs of hematopoietic stem cell aging.Development (Cambridge, England) · 2025Review
- The aging hematopoietic stem cell niche: a mini review.Frontiers in hematology · 2025Article
- G2 arrest primes hematopoietic stem cells for megakaryopoiesis.Cell reports · 2024Article
- Review
- STAT3 protects HSCs from intrinsic interferon signaling and loss of long-term blood-forming activity.bioRxiv : the preprint server for biology · 2023Article
- Impact of Age, Sex, and Genetic Diversity in Murine Models of the Hematopoietic Acute Radiation Syndrome (H-ARS) and the Delayed Effects of Acute Radiation Exposure (DEARE).Current stem cell reports · 2022Article
- Mechanisms involved in hematopoietic stem cell aging.Cellular and molecular life sciences : CMLS · 2022Review
- NF-κB signaling controls H3K9me3 levels at intronic LINE-1 and hematopoietic stem cell genes in cis.The Journal of experimental medicine · 2022Article
- Cellular enlargement - A new hallmark of aging?Frontiers in cell and developmental biology · 2022Review
- Cell size is a determinant of stem cell potential during aging.Science advances · 2021Article
- Molecular and cellular mechanisms of aging in hematopoietic stem cells and their niches.Journal of hematology & oncology · 2020Review
- Hand in hand: intrinsic and extrinsic drivers of aging and clonal hematopoiesis.Experimental hematology · 2020Review
- DNA damage in aging, the stem cell perspective.Human genetics · 2020Review
- Understanding intrinsic hematopoietic stem cell aging.Haematologica · 2020Review
- The lifespan quantitative trait locus geneHaematologica · 2020Article
- Acute Myeloid Leukemia: Aging and Epigenetics.Cancers · 2019Review
- The Phenylethanol Glycoside Liposome Inhibits PDGF-Induced HSC Activation via Regulation of the FAK/PI3K/Akt Signaling Pathway.Molecules (Basel, Switzerland) · 2019Article
- Aging Human Hematopoietic Stem Cells Manifest Profound Epigenetic Reprogramming of Enhancers That May Predispose to Leukemia.Cancer discovery · 2019Article
- Losing Sense of Self and Surroundings: Hematopoietic Stem Cell Aging and Leukemic Transformation.Trends in molecular medicine · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
Whether aged hematopoietic stem and progenitor cells (HSPCs) have impaired DNA damage repair is controversial. Using a combination of DNA mutation indicator assays, we observe a 2- to 3-fold increase in the number of DNA mutations in the hematopoietic system upon aging. Young and aged hematopoietic stem cells (HSCs) and hematopoietic progenitor cells (HPCs) do not show an increase in mutation upon irradiation-induced DNA damage repair, and young and aged HSPCs respond very similarly to DNA damage with respect to cell-cycle checkpoint activation and apoptosis. Both young and aged HSPCs show impaired activation of the DNA-damage-induced G1-S checkpoint. Induction of chronic DNA double-strand breaks by zinc-finger nucleases suggests that HSPCs undergo apoptosis rather than faulty repair. These data reveal a protective mechanism in both the young and aged hematopoietic system against accumulation of mutations in response to DNA damage.
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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.