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已发表论文
外泌体 miR-493-3p 通过抑制白癜风中角质形成细胞的自噬促进 CXCL10 的分泌
Authors Shi Z, Li D, Zhang R, Zeng Y, Liu W, Deng Y
Received 11 September 2025
Accepted for publication 7 December 2025
Published 18 December 2025 Volume 2025:18 Pages 3483—3495
DOI https://doi.org/10.2147/CCID.S566887
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Jeffrey Weinberg
Zeqi Shi,1 Dong Li,1 Ri Zhang,1 Ying Zeng,1 Wenqi Liu,2,* Yunhua Deng1,*
1Department of Dermatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China; 2Division of Parasitology, Department of Pathogen Biology, School of Basic Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yunhua Deng, Department of Dermatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People’s Republic of China, Email 820331158@qq.com Wenqi Liu, Division of Parasitology, Department of Pathogen Biology, School of Basic Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People’s Republic of China, Email liu_wq2002cn@hotmail.com
Background: Vitiligo is a dermatological disorder characterized by the destruction of melanocytes, resulting from a complex interplay of genetic, immune and environmental factors. Recent studies have highlighted the involvement of keratinocytes in the pathogenesis of vitiligo; however, the precise mechanisms underlying this process remain to be fully elucidated. This study aimed to elucidate the specific role of keratinocytes in vitiligo pathogenesis, investigate autophagic changes in lesional keratinocytes, validate miR-493-3p’s regulatory effect on keratinocyte autophagy.
Methods: Initially, the role of keratinocytes in vitiligo lesions were evaluated by reanalyzing single-cell transcriptome data from public databases. Subsequently, a comprehensive analysis of differentially expressed genes was conducted, focusing particularly on changes in the autophagy within keratinocytes. Finally, in vitro studies, including Western Blotting, ELISA, and immunofluorescence assays, were utilized to validate the effects of miR-493-3p on the autophagy, which are implicated in the secretory dysfunction of keratinocytes.
Results: Our study revealed a reduction in the number of keratinocytes in vitiligo lesions, and autophagy was significantly enriched in both WGCNA and KEGG analyses. Additionally, we demonstrated that miR-493-3p directly inhibits the expression of LC3, leading to a decrease in autophagy. Ultimately, we confirmed that autophagy dysfunction results in an increase in CXCL10 levels in keratinocytes, which may be associated with immune-mediated damage to melanocytes.
Conclusion: Our research illustrates the role of keratinocytes in vitiligo and clarifies how miR-493-3p induces secretion dysfunction in keratinocytes by modulating autophagy.
Keywords: vitiligo, keratinocyte, scRNA-seq, miR-493-3p, autophagy
1Department of Dermatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China; 2Division of Parasitology, Department of Pathogen Biology, School of Basic Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yunhua Deng, Department of Dermatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People’s Republic of China, Email 820331158@qq.com Wenqi Liu, Division of Parasitology, Department of Pathogen Biology, School of Basic Sciences, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, People’s Republic of China, Email liu_wq2002cn@hotmail.com
Background: Vitiligo is a dermatological disorder characterized by the destruction of melanocytes, resulting from a complex interplay of genetic, immune and environmental factors. Recent studies have highlighted the involvement of keratinocytes in the pathogenesis of vitiligo; however, the precise mechanisms underlying this process remain to be fully elucidated. This study aimed to elucidate the specific role of keratinocytes in vitiligo pathogenesis, investigate autophagic changes in lesional keratinocytes, validate miR-493-3p’s regulatory effect on keratinocyte autophagy.
Methods: Initially, the role of keratinocytes in vitiligo lesions were evaluated by reanalyzing single-cell transcriptome data from public databases. Subsequently, a comprehensive analysis of differentially expressed genes was conducted, focusing particularly on changes in the autophagy within keratinocytes. Finally, in vitro studies, including Western Blotting, ELISA, and immunofluorescence assays, were utilized to validate the effects of miR-493-3p on the autophagy, which are implicated in the secretory dysfunction of keratinocytes.
Results: Our study revealed a reduction in the number of keratinocytes in vitiligo lesions, and autophagy was significantly enriched in both WGCNA and KEGG analyses. Additionally, we demonstrated that miR-493-3p directly inhibits the expression of LC3, leading to a decrease in autophagy. Ultimately, we confirmed that autophagy dysfunction results in an increase in CXCL10 levels in keratinocytes, which may be associated with immune-mediated damage to melanocytes.
Conclusion: Our research illustrates the role of keratinocytes in vitiligo and clarifies how miR-493-3p induces secretion dysfunction in keratinocytes by modulating autophagy.
Keywords: vitiligo, keratinocyte, scRNA-seq, miR-493-3p, autophagy