Evidence map›Paper›PMID 35932882›Full record

SynthesisAmerican journal of obstetrics and gynecology2023

A systematic review and in silico study of potential genetic markers implicated in cases of overactive bladder.

Ilaha Isali, Phillip McClellan, Thomas R Wong, Clara Sun, Amber Catherine Stout, Fredrick R Schumacher, Sarah Markt, Chen-Han Wilfred Wu, Kathryn L Penney, Sherif El-Nashar and 2 more

Open access · greenAbstract readSystematic Review
In one paragraph

Synthesis in American journal of obstetrics and gynecology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
2.7field-weighted citation impact, top 10% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 12 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 1 country.

Ilaha IsaliDivision of Female Pelvic Medicine and Reconstructive Surgery, Department of Urology, University Hospitals, Cleveland Medical Center, Cleveland, OH.
Phillip McClellanDivision of Female Pelvic Medicine and Reconstructive Surgery, Department of Urology, University Hospitals, Cleveland Medical Center, Cleveland, OH.
Thomas R WongDivision of Female Pelvic Medicine and Reconstructive Surgery, Department of Urology, University Hospitals, Cleveland Medical Center, Cleveland, OH.
Clara SunDivision of Female Pelvic Medicine and Reconstructive Surgery, Department of Urology, University Hospitals, Cleveland Medical Center, Cleveland, OH.
Amber Catherine StoutCore library, University Hospitals, Cleveland Medical Center, Cleveland, OH.
Fredrick R SchumacherDepartment of Population and Quantitative Health Sciences, Case Western Reserve University, Cleveland, OH.
Sarah MarktDepartment of Population and Quantitative Health Sciences, Case Western Reserve University, Cleveland, OH.
Chen-Han Wilfred WuDivision of Female Pelvic Medicine and Reconstructive Surgery, Department of Urology, University Hospitals, Cleveland Medical Center, Cleveland, OH; Department of Genetics and Genome Sciences, Case Western Reserve University, Cleveland, OH.
Kathryn L PenneyDepartment of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA; Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.
Sherif El-NasharDepartment of Obstetrics and Gynecology, Mayo Clinic, Jacksonville, FL.
Adonis HijazDivision of Female Pelvic Medicine and Reconstructive Surgery, Department of Urology, University Hospitals, Cleveland Medical Center, Cleveland, OH.
David SheynDivision of Female Pelvic Medicine and Reconstructive Surgery, Department of Urology, University Hospitals, Cleveland Medical Center, Cleveland, OH. Electronic address: David.Sheyn@uhhospitals.org.
University Hospitals of Cleveland · USCase Western Reserve University · USBrigham and Women's Hospital · USMayo Clinic in Florida · US

Funding

KUH-TN Training CoreTL1DK132770 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI Evi X. Stavrou · 2021 to 2026
$2.5M
NIDDK NIH HHS TL1 DK132770
6 · The paper itself

Abstract

objectiveThe contribution of genetic factors to the presence of an overactive bladder is recognized. This study aimed to (1) assemble and synthesize available data from studies assessing differential gene expression in patients with overactive bladder vs controls without overactive bladder and (2) determine possible correlations and functional pathways between genes. DATA SOURCES: We searched PubMed, Ovid or Medline, and Wiley Cochrane Central Register of Controlled Trials databases between January 1, 2000, and December 15, 2021. STUDY ELIGIBILITY CRITERIA: Studies were included if gene expression was detected and quantified using molecular approaches performed on human bladder tissue specimens directly and excluded if the gene expression analysis was carried out from blood and urine specimens alone.

methodsA systematic review was completed to identify publications that reported differently expressed gene candidates among patients with overactive bladder vs healthy individuals. Gene networking connections and pathway analysis were performed employing Metascape software, where inputs were identified from our systematic review of differentially expressed genes in overactive bladder.

resultsA total of 9 studies were included in the final analysis and 11 genes were identified as being up-regulated (purinergic receptor P2X 2 [P2RX2], smoothelin [SMTN], growth-associated protein 43 [GAP43], transient receptor potential cation channel subfamily M member 8 [TRPM8], cadherin 11 [CDH1], gap junction protein gamma 1 [GJC1], cholinergic receptor muscarinic 2 [CHRM2], cholinergic receptor muscarinic 3 [CHRM3], and transient receptor potential cation channel subfamily V member 4 [TRPV4]) or down-regulated (purinergic receptor P2X 2 [P2RX3] and purinergic receptor P2X 5 [P2RX5]) in patients with overactive bladder. Gene network analysis showed that genes are involved in chemical synaptic transmission, smooth muscle contraction, blood circulation, and response to temperature stimulus. Network analysis demonstrated a significant genetic interaction between TRPV4, TRPM8, P2RX3, and PR2X2 genes.

conclusionOutcomes of this systematic review highlighted potential biomarkers for treatment efficacy and have laid the groundwork for developing future gene therapies for overactive bladder in clinical settings.

Indexed as

Urinary Bladder, OveractiveCholinergic AntagonistsGenetic MarkersHumansReceptor, Muscarinic M3Receptors, CholinergicReceptors, PurinergicTRPV Cation ChannelsCholinergic AntagonistsCHRM3 protein, humanGenetic MarkersReceptor, Muscarinic M3Receptors, CholinergicReceptors, PurinergicTRPV Cation Channelsgene expressiongenomicsoveractive bladdersystematic reviewurge urinary incontinence

Identifiers

PMID35932882
PMCPMC10152473
OpenAlexW4289755521

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.