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- W4285992188 abstract "Hidradenitis suppurativa (HS) is a chronic debilitating disease characterized by inflammatory nodules and sinus tracts in areas rich in terminal hair follicles and apocrine glands. Lifestyle factors associated with oxidative stress, such as obesity and smoking, worsen symptoms. An early step in HS is follicular dilation and occlusion with keratin, which results in follicular rupture and a robust inflammatory response. Nrf2 signaling is a key regulator of follicular response to environmental redox insults and keratin expression. Herein, we utilized indirect immunofluorescence (IF) to assess levels of total and phosphorylated (active) Nrf2 and its inhibitor Keap1 in HS lesional skin (n=10) and sex-matched healthy controls (n=4). There was a decrease of IF signal for all three targets in HS hair follicles compared with controls. Next, we examined whether keratin 16 (K16) may provide a potential mechanistic link between dysfunctional Nrf2 signaling and hyperkeratinization of HS hair follicles. K16 is a stress-inducible target and regulator of Nrf2 signaling. Moreover, K16 overexpression in a tissue-specific transgenic mouse model results in aberrant keratinization of the outer root sheath. We found an upregulation of both K16 and its type II keratin binding partner K6 in the hyperplastic outer root sheath of HS hair follicles and sinus tracts. This suggest that impaired Nrf2 signaling, possibly by virtue of its bidirectional regulatory relationship with K16, may contribute to follicular hyperkeratinization and occlusion in HS. Given growing evidence of the efficacy of topical Nrf2 inducers and attractiveness of early intervention in HS, this work opens up new promising therapeutic avenues for a clinically devastating disease with limited treatment options." @default.
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- W4285992188 date "2022-08-01" @default.
- W4285992188 modified "2023-09-28" @default.
- W4285992188 title "671 Impaired follicular Nrf2 signaling: Potential early therapeutic target in hidradenitis suppurativa" @default.
- W4285992188 doi "https://doi.org/10.1016/j.jid.2022.05.682" @default.
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