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Current insight into the roles of microRNA in vitiligo

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Abstract

Vitiligo is a common chronic depigmented skin disease characterized by melanocyte loss or dysfunction in the lesion. The pathogenesis of vitiligo has not been fully clarified. Most studies have suggested that the occurrence and progression of vitiligo are due to multiple factors and gene interactions in which noncoding RNAs contribute to an individual’s susceptibility to vitiligo. Noncoding RNAs, including microRNAs (miRNAs), are a hot topic in posttranscriptional regulatory mechanism research. miRNAs are noncoding RNAs with a length of approximately 22 nucleotides and play a negative regulatory role by binding to the 3′-UTR or 5′-UTR of the target mRNA to inhibit translation or initiate mRNA degradation. Previous studies have screened the differential expression profiles of miRNAs in the skin lesions, melanocytes, peripheral blood mononuclear cells (PBMCs) and sera of patients and mouse models with vitiligo. Moreover, several studies have focused on miRNA-25, miRNA-155 and other miRNAs involved in melanin metabolism, oxidative stress, and melanocyte proliferation and apoptosis. These miRNAs and regulatory processes further illuminate the pathogenesis of vitiligo and provide hope for the application of small molecules in the treatment of vitiligo. In this review, we summarize miRNA expression profiles in different tissues of vitiligo patients and the mechanisms by which key miRNAs mediate vitiligo development.

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Acknowledgements

Supported by grants from the National Natural Science Foundation of China (NSFC; Grant Nos. 81560502, 81960354), the National Natural Science Foundation of Yunnan Province (Grant No. 2017FB116), the Talent Project of Yunnan Province (2019HB024), 100 Talents Program of Kunming Medical University (Lechun Lyu). The authors acknowledge the editors and reviewers for their positive and constructive comments and suggestions on our study.

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Yan, S., Shi, J., Sun, D. et al. Current insight into the roles of microRNA in vitiligo. Mol Biol Rep 47, 3211–3219 (2020). https://doi.org/10.1007/s11033-020-05336-3

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