Table 3.

Phenotypic and functional aging-related alterations in HSCs and BM niche cells.

Cell Types	Changes with Ageing
HSCs	↑myeloid differentiation; ↓lymphoid differentiation; ↓regenerative potential; ↓HSC polarity; ↓autophagy; ↑deregulated mitochondrial activity; ↑epigenetic and genomic alterations
MSCs	↓CFU-F clonogenicity; ↓Nes–GFP+ and NG2+ cells; ↓CXCR4 →↑ROS production ↑DNA damage→↓ HSCs support; ↑IL6 expression, ↑TGF-β expression →aged HSCs phenotype
ECs	↓ECs number, vascular remodeling → loss of HSC quiescence; ↓key signaling pathways in ECs (mTOR, Jag1/Notch, CXCL12, SCF); ↓HO-1 expression →aged HSC phenotype
OBs	↓ OBs number →↓OPN secretion → aged HSC phenotype; ↓osteogenic progenitor population
MKs	↑ MKs number
Mϕ	↑ Mϕ number; ↑IL-1 secretion→↑HSC myeloid differentiation
ADs	↑ADs number →↓HSCs and progenitors numbers→↓repopulation capacity
Nerve fibers	↓nerve density; ↑β2-adrenergic stimulation ↑→IL6 secretion by MSCs →↑HSC myeloid differentiation

↓—decrease, ↑—increase, →—leads to, HSCs—hematopoietic stem cells, MSCs—mesenchymal stem/stromal cells, ECs—endothelial cells, ADs—adipocytes, MKs—megakaryocytes, OBs—osteoblasts, Mϕ—macrophages.