Abstract

The skin provides an essential barrier against the environment and, therefore, every defect in this tissue has to be rapidly and efficiently repaired. In adult mammals, wounding initiates a well-coordinated sequence of events involving blood clotting and inflammation, new tissue formation, and finally tissue remodeling. The result is a new tissue with a functional skin barrier. However, in adult mammals, wound healing results in formation of a scar, which lacks all appendages and has a reduced tensile strength compared to uninjured skin. By contrast, embryonic skin wounds heal without scar formation and some lower organisms are even capable of completely regenerating the injured tissue. Abnormalities in the wound healing response may lead to excessive healing and formation of hypertrophic scars or keloids. At the other extreme, the repair process is often delayed or completely inhibited, resulting in the development of different types of chronic, nonhealing ulcers. This increases the risk of cancer development at the wound site, in particular under conditions of chronic inflammation. Remarkably, there are striking parallels between wound healing and cancer at the molecular and cellular levels, highlighting the importance of understanding the mechanisms underlying normal and impaired wound healing. Here, we summarize the major events of the wound healing process and the clinical problems associated with impaired wound healing.

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