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).