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    • del Frari, Barbara1
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    • Original Article
      Open Access

      Identification of Keratinocyte Mitogens: Implications for Hyperproliferation in Psoriasis and Atopic Dermatitis

      JID Innovations
      Vol. 2Issue 1100066Published online: October 21, 2021
      • Hanna Niehues
      • Gijs Rikken
      • Ivonne M.J.J. van Vlijmen-Willems
      • Diana Rodijk-Olthuis
      • Piet E.J. van Erp
      • Patrick L.J.M. Zeeuwen
      • and others
      Cited in Scopus: 0
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        Psoriasis and atopic dermatitis are chronic inflammatory skin diseases characterized by keratinocyte (KC) hyperproliferation and epidermal acanthosis (hyperplasia). The milieu of disease-associated cytokines and soluble factors is considered a mitogenic factor; however, pinpointing the exact mitogens in this complex microenvironment is challenging. We employed organotypic human epidermal equivalents, faithfully mimicking native epidermal proliferation and stratification, to evaluate the proliferative effects of a broad panel of (literature-based) potential mitogens.
        Identification of Keratinocyte Mitogens: Implications for Hyperproliferation in Psoriasis and Atopic Dermatitis
      • Original Article
        Open Access

        Peroxisomal Fatty Acid Oxidation and Glycolysis Are Triggered in Mouse Models of Lesional Atopic Dermatitis

        JID Innovations
        Vol. 1Issue 3100033Published online: June 14, 2021
        • Petra Pavel
        • Géraldine Leman
        • Martin Hermann
        • Christian Ploner
        • Thomas O. Eichmann
        • Deborah Minzaghi
        • and others
        Cited in Scopus: 0
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          Alterations of the lipid profile of the stratum corneum have an important role in the pathogenesis of atopic dermatitis (AD) because they contribute to epidermal barrier impairment. However, they have not previously been envisioned as a cellular response to altered metabolic requirements in AD epidermis. In this study, we report that the lipid composition in the epidermis of flaky tail, that is, ft/ft mice mimics that of human lesional AD (ADL) epidermis, both showing a shift toward shorter lipid species.
          Peroxisomal Fatty Acid Oxidation and Glycolysis Are Triggered in Mouse Models of Lesional Atopic Dermatitis
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