Role of MAPK Pathways in the Pathogenesis of Vitiligo

Vitiligo is a chronic, acquired autoimmune disorder characterized by white skin patches resulting from the loss of epidermal melanocytes. Vitiligo may arise through multiple mechanisms, including genetic susceptibility, oxidative stress, autoimmune dysfunction, and environmental factors. Treatment strategies have focused on inhibiting melanocyte loss and stimulating repigmentation. Mitogen-activated protein kinase (MAPK) pathways regulate various cellular processes, including differentiation, survival, and inflammatory responses. The dysregulated MAPK pathways play distinct roles in the development of vitiligo through a complex interplay of melanogenesis, oxidative stress, and autoimmune responses within different cells, thereby leading to melanocyte damage. Thus, therapeutic targeting of MAPK pathways has the potential to mitigate oxidative stress-induced damage and inhibit the exaggerated autoimmunity, thereby controlling disease progression and supporting repigmentation. This review provides an overview of MAPK signaling across the multicellular network in vitiligo pathogenesis and summarizes agents that may provide new perspectives for therapeutic intervention.