ArticleFrontiers in medicine2025
Gain-of-function mutations in KATP channel subunits compromise colonic tight junction integrity and epithelial homeostasis in murine models of Cantú syndrome.
Article in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Introduction: Cantú syndrome (CS) is a rare genetic disorder caused by gain-of-function (GOF) mutations in the Methods: We investigated the effects of CS-associated KATP channel overactivity on epithelial barrier integrity and tight junction (TJ) proteins using murine models. Heterozygous (SUR2 Results: GOF mutations in KATP channels caused significant dysregulation of TJ proteins. Occludin expression was increased in SUR2 Discussion: Our findings demonstrate that CS-associated KATP channel GOF mutations disrupt tight junction dynamics and induces structural remodeling of the colon. This establishes a novel link between KATP channel dysregulation, metabolic-epithelial interactions, and intestinal pathophysiology in CS. Furthermore, the results highlight potential therapeutic targets to mitigate barrier dysfunction, providing a basis for developing interventions to address gastrointestinal symptoms in CS.
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