Antioxidative phytochemicals accelerate epidermal terminal differentiation via the AHR-OVOL1 pathway: Implications for atopic dermatitis

Masutaka Furue, Akiko Hashimoto-Hachiya, Gaku Tsuji

研究成果: ジャーナルへの寄稿 › 評論記事

3 引用 (Scopus)

抄録

Aryl hydrocarbon receptor (AHR) is a chemical sensor that is expressed abundantly in epidermal keratinocytes. Oxidative AHR ligands induce the production of reactive oxygen species. However, antioxidant AHR ligands inhibit reactive oxygen species generation via activation of nuclear factor-erythroid 2-related factor-2, which is a master switch for antioxidative signalling. In addition, AHR signalling accelerates epidermal terminal differentiation, but excessive acceleration by oxidative ligands, such as dioxins, may induce chlo-racne and inflammation. However, antioxidative phytochemical ligands induce the beneficial acceleration of epidermal differentiation that repairs skin barrier disruption. The upregulated expression of differentiation molecules, such as filaggrin, is mediated via the AHR-OVOL1 axis. This AHR-OVOL1 system is capable of counteracting skin barrier dysfunction in T-helper type 2-shifted inflammation. This article reviews the dynamic and multifaceted role of AHR in epidermal biology and discusses the potential use of antioxidative phytochemical ligands for AHR in inflammatory skin diseases, such as atopic dermatitis.

元の言語英語
ページ（範囲）918-923
ページ数6
ジャーナルActa Dermato-Venereologica
巻98
発行部数10
DOI
出版物ステータス出版済み - 10 2018

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Aryl Hydrocarbon Receptors
Phytochemicals
Atopic Dermatitis
Ligands
Reactive Oxygen Species
Inflammation
Skin
Dioxins
Keratinocytes
Skin Diseases
Antioxidants

All Science Journal Classification (ASJC) codes

  • Dermatology

これを引用

Antioxidative phytochemicals accelerate epidermal terminal differentiation via the AHR-OVOL1 pathway : Implications for atopic dermatitis. / Furue, Masutaka; Hashimoto-Hachiya, Akiko; Tsuji, Gaku.

：: Acta Dermato-Venereologica, 巻 98, 番号 10, 10.2018, p. 918-923.

研究成果: ジャーナルへの寄稿 › 評論記事

Furue, M, Hashimoto-Hachiya, A & Tsuji, G 2018, 'Antioxidative phytochemicals accelerate epidermal terminal differentiation via the AHR-OVOL1 pathway: Implications for atopic dermatitis', Acta Dermato-Venereologica, 巻. 98, 番号 10, pp. 918-923. https://doi.org/10.2340/00015555-3003
Furue M, Hashimoto-Hachiya A, Tsuji G. Antioxidative phytochemicals accelerate epidermal terminal differentiation via the AHR-OVOL1 pathway: Implications for atopic dermatitis. Acta Dermato-Venereologica. 2018 10;98(10):918-923. https://doi.org/10.2340/00015555-3003
Furue, Masutaka ; Hashimoto-Hachiya, Akiko ; Tsuji, Gaku. / Antioxidative phytochemicals accelerate epidermal terminal differentiation via the AHR-OVOL1 pathway : Implications for atopic dermatitis. ：: Acta Dermato-Venereologica. 2018 ; 巻 98, 番号 10. pp. 918-923.
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abstract = "Aryl hydrocarbon receptor (AHR) is a chemical sensor that is expressed abundantly in epidermal keratinocytes. Oxidative AHR ligands induce the production of reactive oxygen species. However, antioxidant AHR ligands inhibit reactive oxygen species generation via activation of nuclear factor-erythroid 2-related factor-2, which is a master switch for antioxidative signalling. In addition, AHR signalling accelerates epidermal terminal differentiation, but excessive acceleration by oxidative ligands, such as dioxins, may induce chlo-racne and inflammation. However, antioxidative phytochemical ligands induce the beneficial acceleration of epidermal differentiation that repairs skin barrier disruption. The upregulated expression of differentiation molecules, such as filaggrin, is mediated via the AHR-OVOL1 axis. This AHR-OVOL1 system is capable of counteracting skin barrier dysfunction in T-helper type 2-shifted inflammation. This article reviews the dynamic and multifaceted role of AHR in epidermal biology and discusses the potential use of antioxidative phytochemical ligands for AHR in inflammatory skin diseases, such as atopic dermatitis.",
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