When you get a cut, fibrous connective tissue replaces normal skin, sometimes leaving a visible scar. This process is called fibrosis, and it’s a normal part of the healing process. But sometimes scar formation can be dangerous, disfiguring or just unsightly.
Now Stanford researchers have unraveled how mechanical force contributes to inflammation and scarring in mice, a finding that could potentially lead to new therapies for fibrotic diseases, such as pulmonary fibrosis, and inflammatory diseases, such as rheumatoid arthritis, in humans. Their findings were reported yesterday in Nature Medicine.
“Our study exposes one of the fundamental mechanisms by which the mechanical environment can directly increase inflammation, which is strongly implicated in scarring,” Stanford microsurgeon Geoffrey Gurtner, MD, told me. As I explain in a press release:
Mice genetically engineered to lack an enzyme that is activated by mechanical force demonstrated less inflammation and fibrosis — the formation of excess fibrous connective tissue — in their incisions than mice in a control group, the study found. Inflammation and scar formation also were reduced among mice injected with an organic compound, a small molecule called PF-573228, that blocks this enzyme, which helps cells sense changes in the mechanical environment.
Study results showed that 48 percent fewer scar-tissue cells formed around incisions in mice missing the enzyme than those with the enzyme. Although further testing is needed to determine the validity of the findings in humans, researchers hope the work paves the way for treatment strategies for a variety of diseases that involve inflammation and scarring.