Abstract
Hematopoietic stem cells (HSCs) sustain the lifelong production of all blood cell lineages. The functioning of aged HSCs is impaired, including a declined repopulation capacity and myeloid and platelet-restricted differentiation. Both cell-intrinsic and microenvironmental extrinsic factors contribute to HSC aging. Recent studies highlight the emerging role of inflammation in contributing to HSC aging. In this review, we summarize the recent finding of age-associated changes of HSCs and the bone marrow niche in which they lodge, and discuss how inflammation may drive HSC aging.
Highlights
European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen, Sanquin Research, Landsteiner Laboratory, Amsterdam UMC, 1006 AD Amsterdam, The Netherlands
It seems plausible that the alterations in hematopoiesis during aging are largely due to changes that first occur in the cells from which all blood cells derive, the hematopoietic stem cells
It is evident that stem cell aging is a systemic process, with both intrinsic and extrinsic factors involved
Summary
Multiple aging-associated hematopoietic features occur in both peripheral blood (PB). It seems plausible that the alterations in hematopoiesis during aging are largely due to changes that first occur in the cells from which all blood cells derive, the hematopoietic stem cells. HSCs can undergo both asymmetric and symmetric cell division [9,10] and have the ability to differentiate into multiple mature blood cells and to self-renew, sustaining the stem cell pool throughout life. Whereas young HSCs primarily divide asymmetrically, aged HSCs undergo mainly symmetric divisions [12]. Serial transplantation studies have convincingly demonstrated that aged HSCs display reduced engraftment and self-renewal [1,16,18]. The HSC pool size expands with age, which is considered as a compensatory effect to adjust for the loss of cellular potential
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