ArticleThe Journal of urology2016
The NLRP3 Inflammasome Mediates Inflammation Produced by Bladder Outlet Obstruction.
Article in The Journal of urology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 76 citations in OpenAlex.
- Oxidative stress in bladder outlet obstruction: a narrative review.Translational andrology and urology · 2026Review
- From molecules to the clinic-pathophysiology of sodium-glucose cotransporter 2 inhibitors and their emerging role in urology: A comprehensive review from the European Association of Urology Section of Endourology.Asian journal of urology · 2026Review
- The Interaction Between Mitophagy Dysregulation and the Diabetic Bladder Microenvironment.Journal of diabetes · 2026Review
- TRPA1 promotes overactive bladder progression by activating the NLRP3 inflammasome and driving pyroptosis.Cell death & disease · 2026Article
- Urothelial Piezo1 channel contributes to BOO-induced inflammation, EMT, and bladder fibrosis via activation of NLRP3 inflammasome.Journal of translational medicine · 2026Article
- CD73-Overexpressing ADSCs Promote Neurogenic Bladder Repair via A2A-JAK1/STAT3-Mediated Modulation of Inflammation and Macrophage Polarization.Stem cells international · 2026Article
- IR-780 improves urination function and complications in rats with partial bladder outlet obstruction by protecting bladder smooth muscle cell mitochondria from oxidative stress.Frontiers in pharmacology · 2026Article
- Specialized pro-resolution mediators in the bladder: effects of resolvin E1 on diabetic bladder dysfunction in the type 1 diabetic male Akita mouse model.BMC urology · 2024Article
- Enzyme-induced hypoxia leads to inflammation in urothelial cells in vitro.International urology and nephrology · 2024Article
- Pathophysiology of Overactive Bladder and Pharmacologic Treatments Including β3-Adrenoceptor Agonists -Basic Research Perspectives.International neurourology journal · 2024Article
- The role of inflammasomes in human diseases and their potential as therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Article
- Male Akita mice develop signs of bladder underactivity independent of NLRP3 as a result of a decrease in neurotransmitter release from efferent neurons.American journal of physiology. Renal physiology · 2023Article
- Why Are Some People with Lower Urinary Tract Symptoms (LUTS) Depressed? New Evidence That Peripheral Inflammation in the Bladder Causes Central Inflammation and Mood Disorders.International journal of molecular sciences · 2023Review
- The Urinary Microbiome; Axis Crosstalk and Short-Chain Fatty Acid.Diagnostics (Basel, Switzerland) · 2022Review
- Diabetes causes NLRP3-dependent barrier dysfunction in mice with detrusor overactivity but not underactivity.American journal of physiology. Renal physiology · 2022Article
- CircRNA/miRNA/mRNA axis participates in the progression of partial bladder outlet obstruction.BMC urology · 2022Article
- Diabetic bladder dysfunction progresses from an overactive to an underactive phenotype in a type-1 diabetic mouse model (Akita female mouse) and is dependent on NLRP3.Life sciences · 2022Article
- Flavonoid Nobiletin Attenuates Cyclophosphamide-Induced Cystitis in Mice through Mechanisms That Involve Inhibition of IL-1β Induced Connexin 43 Upregulation and Gap Junction Communication in Urothelial Cells.International journal of molecular sciences · 2022Article
- Specialized pro-resolution mediators in the bladder: Receptor expression and recovery of bladder function from cystitis.Experimental biology and medicine (Maywood, N.J.) · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
purposeWhile bladder outlet obstruction is well established to elicit an inflammatory reaction in the bladder that leads to overactive bladder and fibrosis, little is known about the mechanism by which this is initiated. NLRs (NOD-like receptors) and the structures that they form (inflammasomes) have been identified as sensors of cellular damage, including pressure induced damage, and triggers of inflammation. Recently we identified these structures in the urothelium. In this study we assessed the role of the NLRP3 (NACHT, LRR and PYD domains-containing protein 3) inflammasome in bladder dysfunction resulting from bladder outlet obstruction. MATERIALS AND
methodsBladder outlet obstruction was created in female rats by inserting a 1 mm outer diameter transurethral catheter, tying a silk ligature around the urethra and removing the catheter. Untreated and sham operated rats served as controls. Rats with bladder outlet obstruction were given vehicle (10% ethanol) or 10 mg/kg glyburide (a NLRP3 inhibitor) orally daily for 12 days. Inflammasome activity, bladder hypertrophy, inflammation and bladder function (urodynamics) were assessed.
resultsBladder outlet obstruction increased urothelial inflammasome activity, bladder hypertrophy and inflammation, and decreased voided volume. Glyburide blocked inflammasome activation, reduced hypertrophy and prevented inflammation. The decrease in voided volume was also attenuated by glyburide mechanistically as an increase in detrusor contraction duration and voiding period.
conclusionResults suggest the importance of the NLRP3 inflammasome in the induction of inflammation and bladder dysfunction secondary to bladder outlet obstruction. Arresting these processes with NLRP3 inhibitors may prove useful to treat the symptoms that they produce.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.