process resulting in capillary bed formation. [1,2] However, sprouting angiogenesis can proceed as an overshooting reaction that results in the formation of additional blood vessels, followed by delayed decelerating growth. [3] This decelerating phase occurs simultaneously with the regression of superfluous vessels at a later stage of healing so that vessel beds are pruned back to normal vascular density and vascular homeostasis is maintained; [4] this process is particularly important because uncontrolled vessel growth leads to pathological effects such as proliferative diabetic retinopathy, [5,6] and incorrect vascular patterning causes vessel instability and poor network functionality. [7] Therefore, organized angiogenesis deceleration at the later stage of healing is crucial for vessel normalization and stabilizing the mature vessels, ensuring that tissue regeneration including bone defect healing can be carried out within a controllable range; however, the mechanism behind this remains unclear. Alteration of extrinsic microenvironment, such as hypoxia improvement, is known as a common cause of capillary deceleration, [8,9] yet the decelerating angiogenesis response is usually accompanied by the repairing process of various injured tissue. [10] Therefore, it's reasonable to assume that intrinsic Deceleration of sprouting angiogenesis until its final disappearance after blood vessel reconstruction is crucial for controlled tissue repair; however, its underlying mechanism remains unclear. It is reported that osteogenic differentiated bone marrow stem cells (OD-BMSCs) contribute to sprouting angiogenesis deceleration by releasing intrinsic "OFF" signals. In vitro experiments show that insulin-like growth factor-binding protein 7 (IGFBP7) is the main component of OD-BMSCs paracrine products which could inhibit the tube formation ability of endothelial cells. In addition, cell functional experiments show that IGFBP7 inhibits sprouting angiogenesis by reducing cell migration and tip cell specification. Furthermore, it is found that early IGFBP7 intervention, which accelerates sprouting angiogenesis deceleration during the early stage of healing, impedes bone defect healing. These results demonstrate that OD-BMSCs could offer intrinsic inhibitory signals on sprouting angiogenesis and the appropriate emergence timing of these signals is crucial to maintain vasculature homeostasis during bone repairing. These results provide insight into the complex interaction between osteogenesis-angiogenesis coupling and suggest the potential therapeutic application of IGFBP7 in regulating vascular homeostasis.