331 Mitochondrial stress contributes to atopic dermatitis

Atopic dermatitis (AD) is a complex disease characterized by eczematous lesions over dry skin and local systemic oxidative stress. Indeed, patients with AD display increased concentrations of stress biomarkers in the urine, blood, saliva. Although source ROS uncertain, dysfunctional mitochondria might be involved excessive skin. In this study, we investigated epidermis using mouse model AD, i.e. flaky tail (ft/ft) mice, primary keratinocytes biopsies from patients. We found dysregulated expression genes response keratinocytes. SOD2 cytochrome c were increased, suggesting mitochondrial epidermis. Furthermore, observed down-regulation glutathione system catalase keratinocytes, which lead to accumulation hydrogen peroxide, mainly mitochondria. Moreover, showed an increase malondialdehyde (MDA), 4-hydroxy-2-nonenal (4HNE), oxidized phospholipids Nevertheless, despite low level GPX4 high amount lipid peroxides, ferroptosis intrinsic apoptosis are not triggered MitoQ, but NAC, ameliorates AD-like symptoms ft/ft mice. Thus, indicates that significant could contribute pathogenesis.