ConClusion: Endothelial cell-stromal interactions, mediated by SDF-1, play a pivotal role in maintaining ASC niche transcriptional homeostasis and preserving the functional capacity of ASCs. In the absence of SDF-1, ASCs are shunted towards adipogenesis, with reduced proliferative and proangiogenic capacity, impacting their physiological role within the adipose niche environment and their therapeutic potential in treating ischemia. The dysfunction of ASCs in diabetes may be related to downregulation of SDF-1 and subsequent disruption of the physiological cytokine milieu. Further investigation of the role of SDF-1 in ASC homeostasis and function, particularly in the context of diabetes, is ongoing to inform the development of autologous cell based therapies for diabetic wound healing. 9 Selectively Permeable nanofiber constructs to Prevent inflammatory Scarring and enhance nerve regeneration in Peripheral nerve injury