Fig. 1

The comparison between normal/AML BMM with associated cellular interactions. The composition of the BMM contains hematopoietic cells, several stromal cell populations as well as ECM. HSCs with different behaviors have been found to reside in heterogenous niches. BMM supports hematopoiesis through interactions mediated by cell–cell contact and soluble secreted factors. Compared to normal BMM, there have been several prominent changes in AML BMM, including differential remodeling of the vasculature, alteration of cytokines secretion together with adhesion capacity, adaptability to hypoxia microenvironment and maintenance of low ROS, which lead to AML development and further chemoresistance. AML acute myeloid leukemia, BMM bone marrow microenvironment, HSC hematopoietic stem cell, MSC mesenchymal stem cell, CXCL12 C-X-C motif chemokine 12, CXCR4 C-X-C chemokine receptor 4, VLA-4 very late antigen 4, VCAM-1 vascular cell adhesion molecule 1, TGF-β transforming growth factor-β, OPN osteopontin, G-CSF granulocyte-colony stimulating factor, ECM extracellular matrix, BMA bone marrow Adipose, OB osteoblast OC osteoclast, Ebf3 transcription factor early B-cell factor 3, Foxc1 transcription factor forkhead box C1, HIF hypoxia-inducible factor, VEGF vascular endothelial growth factor, SNS sympathetic nervous system, GFP green fluorescent protein, MSC-EV MSC-derived extracellular vehicles, ROS reactive oxygen species, BCL-2 B-cell lymphoma-2