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Signaling through C-X-C chemokine receptor type 4 (CXCR4), a G-protein-coupled seven transmembrane receptor protein (also known as fusin or CD184), and stromal cell-derived factor 1 (SDF1), a stem cell homing chemokine protein (also known as C-X-C motif chemokine 12/CXCL12),1,2 plays critical roles in controlling the migration and homing of hematopoietic stem cells (HSCs) to their bone marrow niche and regulating their proliferation and repopulation capacities.3 Furthermore, SDF1/CXCR4 signaling also controls the mobilization and migration of mesenchymal stem cells (MSCs) from the bone marrow to sites of injury to prompt tissue/regeneration repair.4 The delineation of pathways that modulate SDF1/CXCR4 signaling and influence hematopoiesis under steady-state and stress-inducing conditions may foster the development of strategies to enhance hematopoietic recovery after hematopoietic injury or improve responses to hematopoietic cell transplantation. Furthermore, an understanding of how diseases such as diabetes influence the SDF1/CXCR4-signaling may allow the modification and significant improvement of stem cell therapies in patients suffering from multiple co-morbidities such as cardiovascular disease and diabetes. In our first Featured Article published this month in STEM CELLS, Chen et al report that the loss of Interferon regulatory factor 7 (Irf7) expression in hematopoietic stem and progenitor cells (HSPCs) boosts stress hematopoiesis in a mechanism involving CXCR4.5 In a Related Article published recently in STEM CELLS Translational Medicine, Mayorga et al demonstrated that diabetes significantly impacted post-acute myocardial infarction (AMI) cardiac repair in diabetic mice by MSCs and that the overexpression of Sdf1 in MSCs rescued their therapeutic capabilities.6

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