Platelets facilitate fat grafting by mitochondrial transfer and reducing oxidative stress in adipose-derived stem cells

Autologous fat grafting (AFG), characterized by a broad tissue source and absence of immune rejection, is extensively utilized in plastic surgery. Despite its advantages, AFG is frequently challenged by a high rate of fat resorption and limited volume retention. Recent studies have increasingly focused on integrating platelet-related preparations with adipose tissue to enhance graft survival rates. These investigations have consistently demonstrated the beneficial effects of platelets and their derivatives on adipose-derived stem cells (ADSCs), facilitating improved outcomes in fat transplantation. Nevertheless, the precise mechanisms governing the interaction between platelets and ADSCs remain insufficiently understood. We investigate the potential of platelets to augment the antioxidant stress capacity of ADSCs through mitochondrial transfer, thereby contributing to enhanced fat graft viability. Experimental results revealed that platelets significantly promoted ADSC proliferation, migration, metabolic activity, and mitochondrial function. Co-culture of oxidative stress-induced ADSCs with platelets resulted in improved cell viability and a marked reduction in reactive oxygen species (ROS) levels. The mitochondrial transfer from platelets to ADSCs, confirmed via fluorescent labeling, played a pivotal role in restoring mitochondrial function and decreasing glucose consumption under stress conditions. Furthermore, in a murine subcutaneous fat graft model, platelets exhibited a protective effect during the early oxidative stress phase, as evidenced by reduced ROS and malondialdehyde levels, increased glutathione expression, attenuated fibrosis, enhanced graft vascularization, and improved long-term survival. These findings suggest that platelet-mediated mechanisms, including mitochondrial transfer, may contribute to protecting ADSCs and improving fat graft outcomes.