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@ARTICLE{Mansell:277462,
author = {E. Mansell and D. S. Lin$^*$ and S. J. Loughran and M.
Milsom$^*$ and J. J. Trowbridge},
title = {{N}ew {I}nsight into the {C}auses, {C}onsequences and
{C}orrection of {H}ematopoietic {S}tem {C}ell {A}geing.},
journal = {Experimental hematology},
volume = {125–126},
number = {September–October 2023},
issn = {0531-5573},
address = {Amsterdam [u.a.]},
publisher = {Elsevier Science},
reportid = {DKFZ-2023-01389},
pages = {1-5},
year = {2023},
note = {#EA:A010#LA:A012# / Volumes 125–126, September–October
2023, Pages 1-5 / Perspective},
abstract = {Ageing of hematopoietic stem cells (HSCs) is characterised
by lineage bias, increased clonal expansion and functional
decrease. At the molecular level, aged HSCs typically
display metabolic dysregulation, upregulation of
inflammatory pathways and downregulation of DNA repair
pathways. Cellular ageing of HSCs, driven by cell-intrinsic
and cell-extrinsic factors, causes predisposition to
anaemia, adaptive immune compromise, myelodysplasia and
malignancy. In fact, most hematological diseases are
strongly associated with age. But what is the biological
foundation for decreased fitness with age? And are there
therapeutic windows to resolve age-related hematopoietic
decline? These questions were the focus of the International
Society for Experimental Hematology New Investigator
Committee Fall 2022 Webinar. This review touches on the
latest insights from two leading laboratories into
inflammatory- and niche- driven stem cell ageing and
includes speculation on strategies to prevent or correct
age-related decline in HSC function (see Fig 1).},
subtyp = {Review Article},
cin = {A010 / A012},
ddc = {610},
cid = {I:(DE-He78)A010-20160331 / I:(DE-He78)A012-20160331},
pnm = {311 - Zellbiologie und Tumorbiologie (POF4-311)},
pid = {G:(DE-HGF)POF4-311},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:37433369},
doi = {10.1016/j.exphem.2023.07.002},
url = {https://inrepo02.dkfz.de/record/277462},
}