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Fig. 2 | Journal of Hematology & Oncology

Fig. 2

From: Mechanisms and rejuvenation strategies for aged hematopoietic stem cells

Fig. 2

Cell-extrinsic mechanisms of HSC aging involved in HSC-surrounding cells (including megakaryocytes, MSCs, macrophages, and neutrophils), cytokines and enzymes (including IL-6, IL-1B, and caspase-1). Disrupted β-adrenergic nerve signaling (increased β2-AR-IL6-mediated megakaryocyte differentiation and reduced β3-AR-Nos1 activity) is an important determinant of niche alterations during aging, resulting in impaired lymphoid differentiation and myeloid expansion. Dysfunction of aged marrow macrophages directs HSC platelet bias; aged mice have markedly more senescent neutrophils and higher levels of cytokines IL-1B and caspase-1 in their BM niche than young mice. The number of MSCs increases significantly during aging and is associated with replicative senescence and HSC homing

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