Activation of TRPV3 Inhibits Lipogenesis and Stimulates Production of Inflammatory Mediators in Human Sebocytes—A Putative Contributor to Dry Skin Dermatoses

    Magdolna Szántó, Attila Oláh, Attila Gábor Szöllősi, Kinga Tóth, Edit Páyer, Nóra Czakó, Ágnes Pór, Ilona Kovács, Christos C. Zouboulis, Lajos Kemény, Tamás Bı́ró, Balázs István Tóth
    TLDR Activating TRPV3 reduces skin oil production and increases inflammation, potentially causing dry skin issues.
    The study revealed that activating TRPV3 in human sebocytes inhibited lipid synthesis and increased the production of inflammatory mediators, suggesting that TRPV3 hyperactivity could contribute to dry skin inflammatory dermatoses. Immunohistochemical analysis confirmed TRPV3 presence in sebaceous glands, and functional assays showed increased intracellular Ca2+ levels upon TRPV3 activation. Using 2-APB and carvacrol, researchers observed reduced lipid synthesis and increased proinflammatory cytokine transcription. RNA interference-based silencing of TRPV3 confirmed its role in these processes. The study proposed TRPV3 as a negative regulator of sebaceous lipid synthesis with proinflammatory effects and recommended further clinical studies on TRPV3 inhibitors for treating inflammatory skin conditions.
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