Okamura Ken, Suzuki Tamio
Department of Dermatology, Faculty of Medicine, Yamagata University, Yamagata, Japan.
Department of Dermatology, Faculty of Medicine, Yamagata University, Yamagata, Japan.
J Dermatol Sci. 2025 Mar;117(3):45-51. doi: 10.1016/j.jdermsci.2025.01.004. Epub 2025 Jan 22.
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.
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，由遗传、表观遗传、免疫和环境因素的复杂相互作用引起。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参与免疫、氧化应激和黑素生成的基因。同时，表观遗传学研究揭示了对白癜风发病机制至关重要的调控网络，重点是DNA甲基化和非编码RNA（如微小RNA、长链非编码RNA和环状RNA）。这些进展为基因调控、免疫过程和细胞动力学提供了更深入的见解。本综述整合了遗传和表观遗传学研究的结果，以全面了解白癜风的分子机制，为创新的个性化治疗方法铺平道路。
