Autophagy in psoriasis and vitiligo

Abstract

Autophagy is a primary catabolic process in eukaryotes which is responsible for degrading dysfunctional and redundant cellular organelles and proteins. The autophagy process plays several roles in maintaining cellular homeostasis, including an endogenous defence mechanism that might play an important role in the development and progression of skin diseases. Psoriasis and vitiligo are common chronic inflammatory skin disorders. Psoriasis is characterized by well-demarcated, erythematous, thickened plaques with an overlying scale. Exact aetiology is complex and influenced by genetic and environmental factors but is not entirely explained. Defects of autophagy in psoriatic skin are likely involved in increased inflammation and disturbed keratinocyte differentiation. Research indicates that autophagy disorders may be associated with various pathways and molecules such as PI3K/AKT/mTOR or toll-like receptors. Vitiligo is characterized by the loss of functional melanocytes. Many hypotheses have been proposed for the pathogenesis of this disease. Autoimmunity and oxidative stress in melanocytes remain the most frequently mentioned. Deregulated autophagy in vitiligo melanocytes might disrupt the antioxidant defence system, which causes melanocytes to have oxidative insults. Still, due to the complexity of this process, its precise role in immune-related inflammatory skin diseases such as psoriasis and vitiligo remains unclear. Objective results will enable the application of new therapeutic strategies.