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Helicobacter pylori infection-induced succinate accumulation drives IBS-D via KAT2A-mediated H3K79 succinylation

ABSTRACT: To explore the molecular mechanisms underlying Helicobacter pylori (Hp)-induced diarrhea-predominant irritable bowel syndrome (IBS-D), C57BL/6 mice were allocated into normal control (NC), Hp-infected, and succinate-treated (SA) groups. Alterations in colonic motility and visceral hypersensitivity were then assessed. Comparative RNA-sequencing (RNA-seq) of colonic tissues was performed to identify differentially expressed genes and elucidate the downstream molecular effectors mediating luminal succinate-driven dysmotility

ORGANISM(S): Mus musculus

PROVIDER: GSE338699 | GEO | 2026/09/03

REPOSITORIES: GEO

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Helicobacter pylori infection-induced succinate accumulation drives IBS-D via KAT2A-mediated H3K79 succinylation

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