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Aryl hydrocarbon receptor impairs HK2-controlled flux of the hexosamine biosynthesis pathway to suppress NETosis in an N-glycosylation-dependent manner.
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ID: paper-40582563
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Aryl hydrocarbon receptor impairs HK2-controlled flux of the hexosamine biosynthesis pathway to suppress NETosis in an N-glycosylation-dependent manner.
Li S, Zhu J, Song J, Yang L, Gong Y et al.
Abstract
INTRODUCTION: The aryl hydrocarbon receptor (AhR) is a promising therapeutic target for ulcerative colitis (UC) and plays a role in regulating neutrophil function. OBJECTIVE: We aimed to investigate the effects and mechanisms of AhR on NETosis, a neutrophil-driven process that disrupts intestinal epithelial homeostasis, to support the development of anti-UC therapies. METHODS: A dextran sulphate sodium (DSS)-induced colitis mouse model was established, and bioinformatics analyses combined with m...
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