ArticleNeurourology and urodynamics2018
NLRP3/IL-1β mediates denervation during bladder outlet obstruction in rats.
Article in Neurourology and urodynamics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 18 citations in OpenAlex.
- 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
- 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
- Human amniotic fluid stem cells can alleviate detrusor dysfunction caused by bladder outlet obstruction in rats.Scientific reports · 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
- Low-Dose Cyclophosphamide Induces Nerve Injury and Functional Overactivity in the Urinary Bladder of Rats.Frontiers in neuroscience · 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
- Expression of Toll-Like Receptors in the Animal Model of Bladder Outlet Obstruction.BioMed research international · 2020Article
- NLRP3/IL1β inflammasome associated with the aging bladder triggers bladder dysfunction in female rats.Molecular medicine reports · 2019Article
- NLRP3 Promotes Diabetic Bladder Dysfunction and Changes in Symptom-Specific Bladder Innervation.Diabetes · 2019Article
- Bladder decompensation and reduction in nerve density in a rat model of chronic bladder outlet obstruction are attenuated with the NLRP3 inhibitor glyburide.American journal of physiology. Renal physiology · 2019Article
- Elevated hydrostatic pressure stimulates ATP release which mediates activation of the NLRP3 inflammasome via P2XInternational urology and nephrology · 2018Article
- Diabetic bladder dysfunction is associated with bladder inflammation triggered through hyperglycemia, not polyuria.Research and reports in urology · 2018Article
Corrections and comments
- Commented on by
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
aimsDenervation of the bladder is a detrimental consequence of bladder outlet obstruction (BOO). We have previously shown that, during BOO, inflammation triggered by the NLRP3 inflammasome in the urothelia mediates physiological bladder dysfunction and downstream fibrosis in rats. The aim of this study was to assess the effect of NLRP3-mediated inflammation on bladder denervation during BOO.
methodsThere were five groups of rats: (i) Control (no surgery); (ii) Sham-operated; (iii) BOO rats given vehicle; (iv) BOO rats given the NLRP3 inhibitor glyburide; and (v) BOO rats given the IL-1 receptor antagonist anakinra. BOO was constructed by ligating the urethra over a 1 mm catheter and removing the catheter. Medications were given prior to surgery and once daily for 12 days. Bladder sections were stained for PGP9.5, a pan-neuronal marker. Whole transverse sections were used to identify and count nerves while assessing cross-sectional area. For in vitro studies, pelvic ganglion neurons were isolated and treated with IL-1β. After a 48 h incubation apoptosis, neurite length and branching were assessed.
resultsIn obstructed bladders, the number of nerves decreased while total area increased, indicating a loss of cell number and/or branching. The decrease in nerve density was blocked by glyburide or anakinra, clearly implicating the NLRP3 pathway in denervation. In vitro analysis demonstrated that IL-1β, a product of the inflammasome, induced apoptosis in pelvic ganglion neurons, suggesting one mechanism of BOO-induced denervation is NLRP3/IL-1β triggered apoptosis.
conclusionsThe NLRP3/IL-1β-mediated inflammation pathway plays a significant role in denervation during BOO.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.