The Aldo-Keto Reductase AKR1B10 Is Up-Regulated in Keloid Epidermis, Implicating Retinoic Acid Pathway Dysregulation in the Pathogenesis of Keloid Disease

    Natalie Jumper, Tom Hodgkinson, Guyan Arscott, Yaron Har‐Shai, Ralf Paus, Ardeshir Bayat
    The study found that the enzyme AKR1B10 was significantly up-regulated in keloid epidermis, suggesting a link between retinoic acid pathway dysregulation and keloid disease pathogenesis. Overexpression of AKR1B10 in normal keratinocytes mimicked the retinoic acid pathway changes seen in keloid epidermis, supporting the hypothesis that AKR1B10 contributes to keloid formation by promoting a profibrotic profile. The research highlighted the potential of targeting AKR1B10 as a therapeutic approach for keloid disease, as current retinoic acid treatments were only partially effective. The study emphasized the importance of epithelial-mesenchymal interactions and suggested that AKR1B10-selective inhibitors could be promising treatments.
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