A new understanding of the molecular pathway in human keloid fibroblasts and development of a novel treatment

This thesis examined the pathophysiology of keloids, a skin disorder caused by abnormal wound healing and scarring, and also developed a novel treatment for the disorder. We found that keloid skin was thicker than normal skin due to the deposition of higher amounts of collagen. Using cells from keloid skin, we also identified that the increased collagen production was induced by abnormal accumulation of a protein, activin, which resulted in keloid scarring. Moreover, a naturally occurring protein, follistatin, blocked the accumulation of activin and was able to prevent keloid fibrosis.