Fig. 7

Graphical abstract of the current study. Schematic illustration of the dysfunctional BM EPCs in HDs, patients with lower-risk MDS, higher-risk MDS and AML. The abilities of BM EPCs from higher-risk MDS patients to support HSCs decreased, whereas to support leukaemia cells increased. Furthermore, BM EPCs might be inclined to induce T cell differentiation towards more immune-tolerant cells in higher-risk MDS patients. In addition, excessive production of ROS and apoptotic pathway activation may be the underlying mechanisms of dysfunctional BM EPCs. AML Acute myeloid leukaemia, BM Bone marrow, EPCs Endothelial progenitor cells, HD Healthy donor, H-MDS Higher-risk myelodysplastic syndromes, HSC Haematopoietic stem cell, L-MDS Lower-risk myelodysplastic syndromes, Th T helper, Tregs T cells, ROS reactive oxygen species