Fig. 1.

Wound healing results from a well-coordinated series of events divided into four overlapping phases: hemostasis, inflammation, proliferation/matrix deposition, and tissue remodeling. Neutrophils and macrophages are particularly important in mediating this process, though T cells and platelets also play key roles. Meanwhile, immune cells themselves release factors such as chemokines and cytokines to amplify inflammatory responses. Next, the inflammatory mediators, such as TGF-β, PDGF, IL-13, IL-6, and IL-4, induce the limited activation and proliferation of myofibroblasts from fibroblasts. In addition to resident fibroblasts, myofibroblasts are derived from multiple cells, including fibrocytes, epithelial cells via EMT, endothelial cells via EndMT, pericyte cells, and smooth muscle cells related to the blood vessels. Activated myofibroblasts migrate to injury sites and stimulate wound closure through cell-generated traction force