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ORIGINAL RESEARCH article

Front. Immunol.

Sec. Autoimmune and Autoinflammatory Disorders : Autoimmune Disorders

This article is part of the Research TopicAdvances in Skin Barrier Dysfunction and Disease PathogenesisView all 4 articles

Yes-associated protein regulates autophagy to restore skin barrier function in atopic dermatitis

Provisionally accepted
Jinjing  JiaJinjing JiaXin  MaXin MaTongfei  WangTongfei WangSiqi  YeSiqi YeFenggen  YanFenggen YanJunfeng  LiuJunfeng LiuHongyi  LiHongyi LiDacan  ChenDacan ChenXiumei  MoXiumei Mo*
  • Department of Dermatology, the Second Clinical College of Guangzhou University of Chinese Medicine, Guangzhou, China

The final, formatted version of the article will be published soon.

Atopic dermatitis (AD) is characterized by skin barrier dysfunction and inflammation. This study explored the relationship between Yes-associated protein (YAP) expression, autophagy, and skin barrier dysfunction in AD. Skin samples from AD patients and healthy controls were analyzed using mRNA-seq. Differential gene expression was visualized using ggplot2 and analyzed using GO and KEGG pathway analyses. An AD mouse model was created using house dust mite ointment, and HaCaT cells were treated to mimic AD inflammation. YAP expression was transfected with lentivirus in vivo and siRNA in vitro. Autophagy was induced with rapamycin. YAP levels were reduced in AD patients and correlated with filaggrin (FLG). YAP overexpression in mice improved skin lesions, enhanced barrier function (increased FLG, involucrin, and loricrin), and promoted autophagy (increased LC3-II/I; decreased p62 and p-mTOR). Similar effects were observed in cells, with increased proliferation and reduced apoptosis. YAP knockdown reversed these effects, which were mitigated by rapamycin. Reduced YAP expression in AD is linked to inflammation and barrier dysfunction. YAP may improve AD by enhancing autophagy, reducing inflammation, and restoring skin barrier function.

Keywords: atopic dermatitis, yes-associated protein, Skin Diseases, Eczematous, Autophagy, Inflammation

Received: 08 Aug 2025; Accepted: 31 Oct 2025.

Copyright: © 2025 Jia, Ma, Wang, Ye, Yan, Liu, Li, Chen and Mo. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Xiumei Mo, moxiumeilsamay@163.com

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