ArticleBJU international2017
cAMP-dependent regulation of RhoA/Rho-kinase attenuates detrusor overactivity in a novel mouse experimental model.
Article in BJU international, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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
3 citing papers in PubMed, 12 citations in OpenAlex.
- Bladder Dysfunction in Sickle Cell Disease Is Associated with Inflammation and Oxidative Stress.International journal of molecular sciences · 2025Article
- Impact of intravascular hemolysis on functional and molecular alterations in the urinary bladder: implications for an overactive bladder in sickle cell disease.Frontiers in physiology · 2024Article
- NO-Releasing Nanoparticles Ameliorate Detrusor Overactivity in Transgenic Sickle Cell Mice via Restored NO/ROCK Signaling.The Journal of pharmacology and experimental therapeutics · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo investigate detrusor function and cAMP activation as a possible target for detrusor overactivity in an experimental model lacking a key denitrosylation enzyme, S-nitrosoglutathione reductase (GSNOR). MATERIALS AND
methodsGSNOR-deficient (GSNOR
resultsGSNOR
conclusionImpaired denitrosylation is associated with detrusor overactivity, which is linked with upregulated RhoA/Rho-kinase signalling. Colforsin reverses physiological and molecular abnormalities. This study describes a novel model of detrusor overactivity and suggests a possible basis for its treatment.
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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.