Evidence map›Paper›PMID 41438679›Full record

ArticleClinical, cosmetic and investigational dermatology2025

Exosomal miR-493-3p Promote the Secretion of CXCL10 by Suppressing Keratinocyte Autophagy in Vitiligo.

Zeqi Shi, Dong Li, Ri Zhang, Ying Zeng, Wenqi Liu, Yunhua Deng

Abstract read
In one paragraph

Article in Clinical, cosmetic and investigational dermatology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

6 authors.

Zeqi ShiDepartment of Dermatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Dong LiDepartment of Dermatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Ri ZhangDepartment of Dermatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Ying ZengDepartment of Dermatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.
Wenqi Liu *Division 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.
Yunhua Deng *Department of Dermatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, People's Republic of China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

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.

Indexed as

autophagykeratinocytemiR-493-3pscRNA-seqvitiligo

Identifiers

PMID41438679
PMCPMC12720970

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.