Mitochondrial Stress Contributes to Atopic Dermatitis

This study explored the role of mitochondrial stress in atopic dermatitis (AD) using a mouse model and samples from AD patients. It found that oxidative stress in AD skin might be linked to dysfunctional mitochondria, as indicated by increased SOD2 and cytochrome c levels. There was also a down-regulation of the glutathione system and catalase, potentially leading to hydrogen peroxide accumulation in mitochondria. Despite increased lipid peroxides, ferroptosis and apoptosis were not triggered. The antioxidant MitoQ improved AD-like symptoms in mice, suggesting mitochondrial stress as a significant source of reactive oxygen species in AD and a contributor to its pathogenesis.