Steroid induced osteonecrosis of the femoral head (SONFH) is a common metabolic disease in clinical practice. However, there are multiple theoretical theories on its pathogenesis, but it is currently believed that microcirculation disorders are the main pathological mechanism causing osteonecrosis of the femoral head. As an immune cell, macrophages play an important role in regulating the balance of tissue microenvironment under normal circumstances. However, the changes in physiological environment after microcirculatory disorders affect the transformation of their metabolic status, resulting in high heterogeneity and plasticity. Especially in the early stages of onset, the impact of vascular growth factor interference on macrophage metabolism on bone resorption and remodeling remains largely elusive. Therefore, investigating the vascular growth factors secreted following microcirculatory disturbances has potential significance in elucidating their role in mediating the pathogenesis of steroid-induced femoral head necrosis via bone immune cells.