Genetics and epigenetics in vitiligo

Ken Okamura, Tamio Suzuki
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Abstract

Vitiligo, a complex autoimmune disorder characterized by melanocyte destruction, arises from an intricate interplay of genetic, epigenetic, immune, and environmental factors. Genome-wide association studies (GWAS) have identified over 50 susceptibility loci, including key genes within the MHC region and those involved in immunity, oxidative stress, and melanogenesis. Concurrently, epigenetic research has unraveled regulatory networks critical to vitiligo pathogenesis, with a focus on DNA methylation and non-coding RNAs (e.g., microRNAs, long non-coding RNAs, and circular RNAs). These advancements provide deeper insights into gene regulation, immune processes, and cellular dynamics. This review integrates findings from genetic and epigenetic studies to offer a comprehensive understanding of molecular mechanisms of vitiligo, paving the way for innovative, personalized therapeutic approaches.
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白癜风的遗传学和表观遗传学。
白癜风是一种以黑素细胞破坏为特征的复杂自身免疫性疾病,是遗传、表观遗传、免疫和环境因素复杂相互作用的结果。全基因组关联研究(GWAS)已经确定了50多个易感位点,包括MHC区域内的关键基因以及与免疫、氧化应激和黑色素生成有关的基因。同时,表观遗传学研究揭示了白癜风发病机制的关键调控网络,重点关注DNA甲基化和非编码rna(如microRNAs、长链非编码rna和环状rna)。这些进步为基因调控、免疫过程和细胞动力学提供了更深入的见解。本文综述了遗传学和表观遗传学研究的结果,以提供对白癜风分子机制的全面了解,为创新的个性化治疗方法铺平道路。
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CiteScore
7.60
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0.00%
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Erratum to "Transcriptional regulation of Mlph and Rab27a by PAX3-NF-κB interaction in melanosome transport of melanocytes" [J. Dermatol. Sci. 120 (2025) 98-104]. SMYD2 promotes oxidative stress-responsive lipid metabolism in melanoma by regulating H3K4 tri-methylation. Editorial board A reappraisal of type 2 cytokine-producing cells in atopic dermatitis: Spotlight on Tc2 cells Transcriptional regulation of Mlph and Rab27a by PAX3-NF-κB interaction in melanosome transport of melanocytes
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