Autophagy in vitiligo: from melanocyte biology to the therapeutic evidence gap

Vitiligo is one of the most common and clinically challenging chronic depigmentary disorders. Current treatments, including corticosteroids, phototherapy, and JAK inhibitors, remain limited by incomplete or non-durable repigmentation, necessitating novel mechanism-based​ therapeutic strategies. Autophagy, classically defined as a lysosomal degradation pathway, is recognized as a key regulator of melanocyte homeostasis, oxidative-stress responses, and immune modulation. Although autophagy has been repeatedly implicated in vitiligo pathogenesis, whether its dysregulation is causal, consequential, or compensatory remains unresolved, and no autophagy-targeted therapy has yet been clinically validated. Here, we stratify current vitiligo therapies by whether their efficacy is directly mediated by melanocyte autophagy, is only indirectly linked to autophagy, or is supported mainly by cross-disease or preclinical evidence. ​Integrating advances in autophagy biology with emerging therapeutic evidence, this review identifies why the therapeutic potential of autophagy in vitiligo remains unvalidated, and outlines the evidence required to test whether autophagy modulation is causally linked to repigmentation.