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Experimental findings show copper chelation reduces visceral hypersensitivity in mice with colitis, suggesting new treatment approaches for IBD.
Our findings for the first time definitely identify and mechanistically elucidate that copper accumulation in the terminal colon and DRG contributes to visceral hypersensitivity in DSS-induced colitis. Dysregulation of the copper transporters ATP7A and CTR1 underlies this copper dyshomeostasis. Our results uncover copper ion homeostasis as a completely unrecognized, novel mechanistic axis driving visceral hypersensitivity in IBD.
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Gao et al. (2026) studied this question.
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