Figure 7.

Mechanism of dermal fibrosis. Deep burn injury activates dermal fibroblasts through TLRs by inflammatory signals derived from infectious pathogens such as LPS and DAMPs, including endogenous molecules such as denatured ECM. Activated fibroblasts, in turn, release chemokines such as SDF-1, which leads to the recruitment of blood-borne cells into wounds. These cells may be the progenitor cells of macrophages and fibrocytes, and they contribute to hypertrophic scarring by directly differentiating to fibroblasts and myofibroblasts, or indirectly regulating fibroblasts to fibrosis by many growth factors, including TGF-β. DAMPs, damage-associated molecule pathogens; LPS, lipopolysaccharide; TGF, transforming growth factor; TLR, toll-like receptor. To see this illustration in color, the reader is referred to the web version of this article at www.liebertpub.com/wound