Senescence and functional failure in hematopoietic stem cells

Chen, Jichun

doi:10.1016/j.exphem.2004.08.001

Cited by 53Hematopoietic Stem Cell TransplantationTelomeres, Telomerase, and SenescenceMesenchymal stem cell research

Senescence and functional failure in hematopoietic stem cells

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Chen, Jichun·2004·Experimental Hematology

DOI 10.1016/j.exphem.2004.08.001

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Abstract

Maintaining normal function of hematopoietic stem cells (HSCs) is critical to blood coagulation, oxygen transportation, and host defense against infection. A potential cause of HSC dysfunction is senescence, in which HSCs and progenitor cells suffer from proliferative arrest. Studies on humans and various animal models have indicated that HSCs can become senescent, showing a significant decline in functional ability with increasing age. There are genetic elements mapped to specific chromosomal sites that regulate HSC senescence. These elements may differ among species, strains, and even individuals. HSC senescence and related pathological effects may not be obvious during normal lifetime under most circumstances since individual primitive HSC clones can function long-term to produce progeny that sustain life-long mature blood cell production. Shortening of telomeres at the chromosomal ends could contribute to HSC senescence, especially when HSCs are stressed under certain pathological conditions. Future studies should define the molecular elements that are important in the regulation of HSC senescence.

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Many adult stem or progenitor cells do not proliferate indefinitely, whether mouse or human in origin.
“However, many adult stem or progenitor cells do not proliferate indefinitely, whether mouse or human in origin (Geiger and Van Zant, 2002; Chen, 2004; Park et al., 2004; Villa et al., 2004).”
From Senescent cells, tumor suppression, and organismal aging: good citizens, bad neighbors (2005) · cites this paper as Chen, 2004

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Authors: Chen, J.
Affiliations: National Institutes of Health (US)
Corresponding author: Chen, Jichun
ORCID: Chen, Jichun
Venue: Experimental Hematology
Publisher: Elsevier BV
Published: 2004-11
Volume: 32
Issue: 11
Pages: 1025-1032
ISSN: 0301-472X (ISSN-L)
DOI: 10.1016/j.exphem.2004.08.001
OpenAlex: W2107768040
Cited by: 53
References: 76
Citations by year: 2025: 1 · 2023: 1 · 2022: 2 · 2021: 1 · 2017: 3 · 2015: 2 · 2014: 1 · 2013: 2 · 2012: 6
FWCI: 0.46
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
www.elsevier.com/open-access/userlicense/1.0/ (vor, 6428 d)
Locations: Experimental Hematology (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Hematology › Hematopoietic Stem Cell Transplantation
Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
Health Sciences › Medicine › Genetics › Mesenchymal stem cell research
Keywords: hematopoietic stem cells, cellular senescence, telomere shortening, aging, proliferative arrest, chromosomal loci, hematopoiesis, stem cell maintenance
MeSH terms: Animals, Clone Cells, Hematopoietic Stem Cells, Humans, Telomere, Cellular Senescence, Cell Proliferation

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Senescence and functional failure in hematopoietic stem cells

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