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Vitiligo is an acquired pigmentary disorder characterized by areas of depigmented skin resulting from loss of epidermal melanocytes. The cause of the destruction of epidermal melanocytes is complex and not yet fully understood. However, there are several hypotheses related to biochemical, neural and genetic aspects as well as oxidative stress and autoimmune mechanisms proposed to understand this disorder. Oxidative stress has a role in vitiligo onset, while autoimmunity contributes to disease progression. In this review, we discuss the mechanisms that link triggering factors with the disease progression. Oxidative stress causes disruption in redox potentials that extend to the Endoplasmic Reticulum (ER), causing accumulation of misfolded proteins, which activates the Unfolded Protein Response (UPR). Melanocytes at the periphery of vitiligo lesions show dilation of the ER. Following exposure to various triggers of vitiligo melanocytes produce cytokines that activate immune response. These studies expand our understanding of the possible underlying mechanisms of melanocyte loss in vitiligo pathogenesis highlighting the possible mechanisms linking ER stress to oxidative stress and autoimmunity.

Could ER Stress Be A Major Link Between Oxidative Stress And Autoimmunity In Vitiligo?