Similar mechanisms may also be activated in a damaged and fibrotic urothelium that fails to perform its barrier function or maintain normal activity, which could potentially lead to detrusor overactivity (Ferguson et al., 2015; Avci et al., 2024) To address this mechanistic hypothesis, our future investigations will systematically dissect the spatiotemporal dynamics of TRPC3-dependent Ca2+ oscillations and their molecular crosstalk with TGF-β/Smad phosphorylation cascades within the fibrotic bladder microenvironment characteristic of IC/BPS. This evidence concerns the gene TRPC3 and Bartsocas-Papas syndrome 1.