ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2026
Dysregulation of CD39/Ectonucleoside Triphosphate Diphosphohydrolase 1 Causes Urinary Bladder Dysfunction with Abnormal Smooth Muscle Contractility.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2026. 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
Lower urinary tract symptoms (LUTS) are prevalent among the aging population, and current medications offer limited efficacy. Improved therapies require a better understanding of the mechanisms underlying LUTS. Abnormal extracellular ATP levels and altered purinergic contractility have been reported in patients with LUTS, suggesting dysregulation of the purinergic pathways. CD39/ENTPD1 is a major regulator of purinergic metabolism, and patients with ENTPD1 loss-of-function mutations exhibit bladder hypomotility and incontinence, suggesting critical roles for ENTPD1 in bladder function. We have tested this hypothesis in an overexpression mouse model with human ENTPD1 knock-in (hCD39TG), in a hemizygous Entpd1 mouse model (Entpd1
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