Keratinocyte-Derived Follistatin Regulates Epidermal Homeostasis and Wound Repair

In this study, researchers generated mice lacking the activin antagonist follistatin in keratinocytes to explore the effects of targeted activin activation in the epidermis and hair follicles. They observed enhanced keratinocyte proliferation in the tail epidermis and an earlier onset of keratinocyte hyperproliferation at the wound edge in these mutant mice, leading to an enlarged hyperproliferative epithelium after skin injury. Despite these changes, granulation tissue formation and scarring were not affected, indicating that selective activation of activin in the epidermis enhances reepithelialization without compromising the quality of the healed wound.