Advances of Stem Cell Therapeutics in Cutaneous Wound Healing and Regeneration

Figure 1

Graphical presentation of stem cell-mediated effect on refractory wound healing process. (a) Phase I: in inflammatory phase, the wound bed contains a large number of neutrophils, early phase macrophages, platelet plugs, and fibrin clots. Initiation of healing process occurs at this phase. (b) Phase II, A: systemic or local administration of stem cell homed to the wound bed. Exogenous stem cells mobilize host resident stem cells to take part in the healing process in GT formation by facilitating angiogenesis. Exogenous stem cells also directly take part in this healing process. The surrounding mobilized fibroblasts also differentiate into myofibroblasts and with collagen deposition facilitate reepithelialization process. B: in the absence of stem cell therapy, inflammatory cells such as neutrophils and macrophages still remain within the wound bed and impaired recruitment of endogenous stem cells occurs, which mediate an imbalance in the orchestrated harmony. GT formation is hindered due to the lack of angiogenesis, myofibroblast differentiation, collagen deposition, and reepithelialization. (c) Phase III: stem cell therapy generates scar tissue within the wound by replacing the provisional matrix. However, without stem cell therapy, refractory condition remains. The wound bed remains enriched with inflammatory cells and their proinflammatory secretory products. IL: interleukin; VEGF: vascular endothelial growth factor; PDGF: platelet-derived growth factor; TGF-β: transforming growth factor beta; MMP: matrix metalloproteinase.

(a)

(b)

(c)