ReviewInternational journal of hematology2005
Senescence of hematopoietic stem cells and bone marrow failure.
Review in International journal of hematology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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
5 citing papers in PubMed.
- TopBP1 Governs Hematopoietic Stem/Progenitor Cells Survival in Zebrafish Definitive Hematopoiesis.PLoS genetics · 2015Article
- Recent insights into the molecular mechanisms involved in aging and the malignant transformation of adult stem/progenitor cells and their therapeutic implications.Ageing research reviews · 2009Review
- Molecular chaperones regulate p53 and suppress senescence programs.FEBS letters · 2007Review
- Inflammatory ROS promote and cooperate with the Fanconi anemia mutation for hematopoietic senescence.Journal of cell science · 2007Article
- Telomerase RNA level limits telomere maintenance in X-linked dyskeratosis congenita.Genes & development · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Functional failure in hematopoietic stem cells (HSCs) may bring fatal consequences because HSCs are the ultimate source of mature blood cells, which need continuous replenishment. One potential cause of HSC dysfunction is senescence, in which HSCs and progenitor cells enter a state of proliferative arrest. HSC senescence is genetically regulated and one particular regulator is the telomerase gene. Mutations in the telomerase gene complex have been found in patients with bone marrow failure syndromes. During a normal lifetime, HSC clones function over the long term and may not show any functional loss under normal circumstances. However, pathologic environments may limit HSC proliferation, accelerate HSC turnover, and shorten the functional life of HSCs, leading to HSC clonal exhaustion and senescence.
Indexed as
Identifiers
16207589What 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.