From the paper: "We identified two chemicals—Y27632 and apocynin—that induced COL17A1 expression in keratinocytes. To test whether these compounds increased th

From the paper: "We identified two chemicals—Y27632 and apocynin—that induced COL17A1 expression in keratinocytes. To test whether these compounds increased the self-renewing capabilities of epidermal stem cells in vitro, we performed colony-formation assays40,41; Y-27632 increased colony number, and both drugs increased colony size (Extended Data Fig. 9m–p). Application of these drugs to full-thickness skin wounds significantly promoted wound repair, similarly to the effect of overexpression of human COL17A1 in mice (Extended Data Fig. 9q–s). Collectively, these data show that COL17A1-inducing drugs promote skin wound healing through re-epithelization of the wound edge with epidermal stem cell expansion, and point towards directions for facilitating skin regeneration and reducing skin ageing." It seems like one very promising application could be in promoting wound healing in certain populations e.g. venous stasis ulcers, pressure ulcers, and many other chronic wounds that don't heal well especially in the elderly (if the treatment were safe). That would be fantastic. But the use of the term anti-aging effects in this paper is suspect. COL17A is part of the basement membrane holding together the thin epidermis and thicker underlying dermis, whereas much aging related research that focuses on 'collagen' loss relates to the amount of collagen I in the thicker underlying dermis. Loss of dermal collagen I with aging is associated with cosmetic changes like thin skin (dermal thinning) and wrinkling. It would be surprising if increased expression of COL17A1 at the basement membrane dramatically induced cosmetic anti-aging effects in the sense of increased level of collagen I in the dermis. Also, it may be a band-aid for one particular cellular function that is important for local tissue structure and cell functions, but the underlying causes of general aging change in cells (mutation accumulation, UV damage, oxidative damage, etc) probably are not being addressed or reversed.