Curr Opin Immunol. 2025 May 30;95:102580. doi: 10.1016/j.coi.2025.102580. Online ahead of print.
ABSTRACT
Vitiligo, characterized by epidermal melanocytes loss causing skin depigmentation, affects millions globally. This review explores its pathogenesis, emphasizing the role of epigenetic mechanisms such as DNA methylation, histone modification, noncoding RNAs, chromatin remodeling, and 3D genome regulation. These mechanisms interact with genetic and environmental factors, contributing to melanocyte destruction. DNA methylation dysregulation, particularly in genes such as TYR and POMC, disrupts melanocyte homeostasis. Histone modification imbalances, including excessive histone deacetylase (HDAC) activation, promote melanocyte apoptosis. Noncoding RNAs, such as miR-211 and lncRNAs, regulate gene expression and immune responses. Chromatin remodeling and 3D genome interactions further influence gene expression, impacting melanogenesis. Despite advancements, challenges remain, including sample heterogeneity, limited model systems, and data integration complexities. Future directions include multiomics studies, organoid models, and personalized treatments. Epigenetic drugs like HDAC inhibitors and CRISPR-dCas9 show promise, with combination therapies offering synergistic effects. This review underscores the potential of epigenetics in advancing vitiligo research and clinical applications.
PMID:40449043 | DOI:10.1016/j.coi.2025.102580