Evidence map›Paper›PMID 26926557›Full record

ArticleThe Journal of urology2016

Inhibition of HIF Reduces Bladder Hypertrophy and Improves Bladder Function in Murine Model of Partial Bladder Outlet Obstruction.

Nao Iguchi, Anna P Malykhina, Duncan T Wilcox

Open access · greenAbstract read
In one paragraph

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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.0field-weighted citation impact, top 16% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

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  5. [Establishment of an Animal Model of Vesicoureteral Reflux Renal Injury through Partial Bladder Outlet Obstruction].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2021
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  15. Evaluation of HIF-1α and VEGF-A expression in radiation-induced cystitis: A case-control study.International braz j urol : official journal of the Brazilian Society of Urology
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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

3 authors at 2 institutions in 1 country.

Nao IguchiDivision of Urology, Department of Surgery, University of Colorado School of Medicine, Aurora, Colorado.
Anna P MalykhinaDivision of Urology, Department of Surgery, University of Colorado School of Medicine, Aurora, Colorado.
Duncan T WilcoxDivision of Urology, Department of Surgery, University of Colorado School of Medicine, Aurora, Colorado; Children's Hospital Colorado, Aurora, Colorado. Electronic address: Duncan.Wilcox@childrenscolorado.org.
University of Colorado Denver · USChildren's Hospital Colorado · US

Funding

University of Colorado Cancer Center Support Grant - Lung Cancer Patient-Derived Xenografts with Autologous Human Immune SystemsP30CA046934 · NCI · UNIVERSITY OF COLORADO DENVER · PI James V Degregori · 1988 to 2026
$117.0M
Role of Mechanotransduction in detrusor over activityR01DK095817 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI MALYKHINA, ANNA P · 2014 to 2017
$1.2M
NCI NIH HHS P30 CA046934NCI NIH HHS P30CA046934NIDDK NIH HHS R01 DK095817
6 · The paper itself

Abstract

purposePosterior urethral valves are the most common cause of partial bladder outlet obstruction in the pediatric population. However, to our knowledge the etiology and the detailed mechanisms underlying pathological changes in the bladder following partial bladder outlet obstruction remain to be elucidated. Recent findings suggest that hypoxia and associated up-regulation of HIFs (hypoxia-inducible factors) have a key role in partial bladder outlet obstruction induced pathology in the bladder. We examined the effects of pharmacological inhibition of HIF pathways by 17-DMAG (17-(dimethylaminoethylamino)-17-demethoxygeldanamycin) in pathophysiological phenotypes after partial bladder outlet obstruction. MATERIALS AND

methodsPartial bladder outlet obstruction was surgically created in male C57BL/6J mice. The animals received oral administration of 17-DMAG or vehicle daily starting from the initiation of obstruction up to 5 days. Sham operated mice served as controls. Bladders were harvested from each group 2, 4 and 7 days postoperatively, and analyzed for histological and biochemical changes. Bladder function was assessed by in vitro muscle contractility recordings.

resultsPartial bladder outlet obstruction caused a significant increase in the bladder mass accompanying enhanced collagen deposition in the bladder wall while 17-DMAG treatment suppressed those increases. Treatment with 17-DMAG attenuated the degree of up-regulation of HIFs and their target genes involving the development of tissue fibrosis in obstructed bladders. Treatment with 17-DMAG improved the decreased responses of obstructed bladder strips to electrical field stimulation and KCl.

conclusionsIn vivo 17-DMAG treatment decreased partial bladder outlet obstruction induced pathophysiological changes in the bladder. HIF pathway inhibition has a potential clinical implication for the development of novel pharmacological therapies to treat bladder pathology associated with partial bladder outlet obstruction.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsBenzoquinonesDisease Models, AnimalEndothelial PAS Domain-Containing Protein 1HypertrophyLactams, MacrocyclicMaleMiceMice, Inbred C57BLUrinary BladderUrinary Bladder Neck Obstruction17-(dimethylaminoethylamino)-17-demethoxygeldanamycinBasic Helix-Loop-Helix ProteinsBenzoquinonesEndothelial PAS Domain-Containing Protein 1Lactams, Macrocyclic17-(dimethylaminoethylamino)-17-demethoxygeldanamycinanoxiahypoxia-inducible factor 1musclesmoothurinary bladder neck obstruction

Identifiers

PMID26926557
PMCPMC5505069
OpenAlexW2274110972

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.