Vitiligo and Epigenetics: From Pathogenesis to Clinical Applications

Vitiligo is a multifactorial chronic depigmentary disorder characterised by the loss of functional melanocytes. Its pathogenesis involves complex interactions among genetic predisposition, environmental factors, and autoimmune dysregulation. In recent years, extensive research has highlighted the critical role of epigenetic regulation in vitiligo development, including aberrant DNA methylation, dysregulated histone modifications, and non-coding RNA (ncRNA) expression disturbances. These abnormal epigenetic modifications contribute to disease progression by disrupting melanogenesis, promoting oxidative stress-induced melanocyte apoptosis, and driving autoimmune responses. From a translational perspective, specific epigenetic alterations show potential as diagnostic biomarkers, disease severity indicators, and therapeutic response monitors. Furthermore, epigenetic drugs, CRISPR/dCas9-based epigenetic editing, and targeted epigenetic reprogramming of tissue-resident memory T cells demonstrate promising clinical applications. This review systematically summarises the molecular mechanisms underlying epigenetic dysregulation in vitiligo pathogenesis and explores its translational implications, providing a theoretical foundation for advancing disease understanding and developing novel therapeutic strategies.