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- Academic Editors
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Background: Diabetic bladder dysfunction (DBD) is driven in part by
inflammation which dysregulates prostaglandin release in the bladder. Precise
inflammatory mechanisms responsible for such dysregulation have been elusive.
Since prostaglandins impact bladder contractility, elucidating these mechanisms
may yield potential therapeutic targets for DBD. In female Type 1 diabetic Akita
mice, inflammation mediated by the nucleotide-binding domain,
leucine-rich–containing family, pyrin domain–containing-3 (NLRP3) inflammasome
is responsible for DBD. Here, we utilized female Akita mice crossbred with
NLRP3 knock-out mice to determine how NLRP3-driven inflammation impacts
prostaglandin release within the bladder and prostaglandin-mediated bladder
contractions. Methods: Akita mice were crossbred with
NLRP3