Prompt wound healing and closure are key to preventing subsequent scars and contractures, as well as eliminating systemic infections such as burn wound sepsis and even shock (Hughes et al., Burns 47:349–370, 2021). Hypertrophic scars or keloidKeloid scars caused by burns are sometimes problematic when functional regions such as articular joints or conspicuous areas on the face or extremities are involved (Edgar and Brereton, BMJ 329:343–345, 2004). Massive burn wound scars have a tendency to develop progressive hypertrophic scars, and earlier skin grafting may improve the overall skin quality as well as shorten the hospital stay (Fujii, Acta Chir Plast 32:46–56, 1990). Humoral and cellular mediators have been considered for the pathogenesis of burn wound-induced hypertrophic scars. One possible role of the growth factors or cytokines in wound healing is to promote high cellular proliferation, differentiation, and migration of keratinocytesKeratinocytes of the epidermisEpidermis and the recruitment of inflammatory cellsInflammatory cells (Kibe et al., Br J Dermatol 143:720–727, 2000). A basic fibroblast growth factor (bFGF)Basic fibroblast growth factor (bFGF) may play a pivotal role in cutaneous wound healing by activating local macrophages, with the effects continuing up to the remodelingRemodeling stage, several weeks after the initial injury. Burn wound fluids or skin graftSkin graft wound fluids limited to the dermisDermis contain lower concentrations of bFGFBasic fibroblast growth factor (bFGF) compared to surgical wounds, which are deeper than the dermis with subsequently lower endothelial cell proliferative and chemotactic activities (Nissen et al., J Trauma 54:1205–1210, 2003). The bFGFBasic fibroblast growth factor (bFGF) is increased by siliconeSilicone gel application in normal and fetal fibroblastFibroblast cultures and may result in the prevention of hypertrophic scars. The healing of burn wounds is more complicated than acute wound healing. Sustained burn wounds are more susceptible to bacterial contamination and bring about unfavorable results, particularly in children (Akita et al., J Burn Care Res 27:333–338, 2006). Faster wound healing is highly expected to prevent severe systemic damage or sequelae such as invasive wound infectionInfection and sepsis. The bFGFBasic fibroblast growth factor (bFGF) was effective for second-degree burn wound healing in a randomized control trial, although bovine recombinant bFGFBasic fibroblast growth factor (bFGF) was employed (Fu et al., Lancet 352:1661–1664, 1998). The bFGFBasic fibroblast growth factor (bFGF) was regulated in spatial and temporal expression in accordance with the recruitment of inflammatory cellsInflammatory cells and interaction with keratinocytesKeratinocytes (Kibe et al., Br J Dermatol 143:720–727, 2000) and was lower in second-degree burn wound fluid, therefore decreasing endothelial cell proliferative and chemotactic activity (Nissen et al., J Trauma 54:1205–1210, 2003). Wounds treated with bFGFBasic fibroblast growth factor (bFGF) produced scars that were significantly less hard 1 year after final wound closure (Akita et al., Burns 31:855–858, 2005).