1. SAT in wound healing
Wound healing consists of several regenerative phases (Fig 3), in which keratinocytes act as the main effectors by supporting fibroblasts, leukocytes, and mesenchymal cells (37). SAT-based processes play an essential role in all phases of wound healing via the secretion of glucocorticoids, adipokines (e.g., interleukins (IL)-1β, -6,-8,-10; leptin, adiponectin, MCP-1, TNF), and other bioactive molecules (e.g., vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), transforming growth factor beta (TGFβ) (38-41). In a mouse model, dermal adipocytes played a crucial role in initiating inflammation post-injury contributed to wound repair by dedifferentiating into myofibroblasts, for extracellular matrix (ECM) production (32, 42). A particularly important role in wound healing has been attributed to ASCs. ASCs promote cutaneous neovascularization and re-epithelialization through secretion of growth factors and cytokines (43-45). Several pre-clinical studies have shown the potential therapeutic effect of ASCs in wound repair (46, 47). Despite ASCs being considered a relatively safe source of stem cells, their widespread therapeutic application is currently hindered by barriers such as cost and the absence of highly standardized cell preparation methodologies (46). As an alternative to ASC-based cell therapy, the administration of ASC-derived exosomes (48-50) has been explored, demonstrating immunomodulatory effects and the ability to promote angiogenesis and re-epithelization (51, 52) (Fig 3a).