ArticleAmerican journal of physiology. Renal physiology2019
Bladder decompensation and reduction in nerve density in a rat model of chronic bladder outlet obstruction are attenuated with the NLRP3 inhibitor glyburide.
Article in American journal of physiology. Renal physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Noninvasive monitoring of lower urinary tract dysfunction in rats with bladder outlet obstruction using uroflowmetry and ultrasonography.International urology and nephrology · 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
- Can Urinary Bladder Innervation Be Restored After Outlet Obstruction and Denervation?International neurourology journal · 2024Article
- New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Review
- Pathophysiology of Overactive Bladder and Pharmacologic Treatments Including β3-Adrenoceptor Agonists -Basic Research Perspectives.International neurourology journal · 2024Article
- 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
- Anti-fibrotic effect of tocotrienols for bladder dysfunction due to partial bladder outlet obstruction.Investigative and clinical urology · 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
- Diabetes causes NLRP3-dependent barrier dysfunction in mice with detrusor overactivity but not underactivity.American journal of physiology. Renal physiology · 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
- Inflammation triggered by the NLRP3 inflammasome is a critical driver of diabetic bladder dysfunction.Frontiers in physiology · 2022Review
- Specialized proresolution mediators in the bladder: annexin-A1 normalizes inflammation and bladder dysfunction during bladder outlet obstruction.American journal of physiology. Renal physiology · 2021Article
- BOO induces fibrosis and EMT in urothelial cells which can be recapitulated in vitro through elevated storage and voiding pressure cycles.International urology and nephrology · 2021Article
- Neurophysiological control of urinary bladder storage and voiding-functional changes through development and pathology.Pediatric nephrology (Berlin, Germany) · 2021Review
- In utero and lactational PCB exposure drives anatomic changes in the juvenile mouse bladder.Current research in toxicology · 2021Article
- A possible mechanism underlying mood disorders associated with LUTS: Chronic bladder outlet obstruction causes NLRP3-dependent inflammation in the hippocampus and depressive behavior in rats.Neurourology and urodynamics · 2020Article
- Review
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6 authors at 1 institution in 1 country.
Funding
Abstract
Bladder outlet obstruction (BOO) leads to progressive voiding dysfunction. Acutely, obstruction triggers inflammation that drives bladder dysfunction. Over time, inflammation leads to decreased bladder nerve density and increased fibrosis, responsible for eventual decompensation and irreversibility. We have previously shown that BOO triggers inflammation, reduced bladder nerve density and increased fibrosis via activation of the NLRP3 inflammasome in an acutely obstructed (12-day) rat model. However, as BOO progresses, the bladder may become decompensated with an increase in postvoid residual volume and decreased voiding efficiency. Currently, we have examined rat bladder function and nerve densities after chronic BOO to determine whether NLRP3 plays a role in the decompensation at this stage. Four groups were examined: control, sham-operated, BOO, or BOO+gly (glyburide; an NLRP3 inhibitor). After 42 days, bladder weight, inflammation (Evans blue), urodynamics, and nerve density were measured. BOO greatly enhanced bladder weights and inflammation, while inflammation was prevented by glyburide. Voiding pressures were increased, and flow rates decreased in BOO and BOO+gly groups, demonstrating physical obstruction. No difference in frequency or voided volume was detected. However, postvoid residual volumes were greatly increased in BOO rats while BOO+gly rats were not different than controls. Moreover, there was a dramatic decrease in voiding efficiency in the chronic BOO rats, which was prevented with glyburide treatment. Finally, a reduction in nerve density was apparent with BOO and attenuated with glyburide. Together the results suggest a critical role for NLRP3 in mediating bladder decompensation and nerve density during chronic BOO.
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