Evidence map›Paper›PMID 27824068›Full record

ArticleScientific reports2016

Sulforaphane Improves Ischemia-Induced Detrusor Overactivity by Downregulating the Enhancement of Associated Endoplasmic Reticulum Stress, Autophagy, and Apoptosis in Rat Bladder.

Huai-Ching Tai, Shiu-Dong Chung, Chiang-Ting Chien, Hong-Jeng Yu

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

11 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Anticarcinogenic Effects of Isothiocyanates on Hepatocellular Carcinoma.International journal of molecular sciences · 2022
    Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. The Role of Apoptosis in Detrusor Contractility.International neurourology journal · 2020
    Article
  8. Review
  9. Article
  10. Article
  11. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Huai-Ching TaiDepartment of Urology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
Shiu-Dong ChungGraduate Institution of Clinical Medicine, National Taiwan University College of Medicine, Taipei, Taiwan.
Chiang-Ting ChienDepartment of Life Science, National Taiwan Normal University, Taipei, Taiwan.
Hong-Jeng YuDepartment of Urology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
National Taiwan University Hospital · TWFar Eastern Memorial Hospital · TWNational Taiwan Normal University · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis-associated pelvic ischemia has been reported to be a risk factor for bladder dysfunction and subsequent lower urinary tract symptoms (LUTS) in the elderly population. However, the molecular mechanisms of this association remain unclear. We hypothesized that stress-induced cellular responses might play a role in the pathogenesis of ischemia-induced bladder dysfunction. In the present study, the animal model of bladder ischemia was induced by bilateral partial arterial occlusion (BPAO) in rats. We found that BPAO significantly induced the presence of detrusor overactivity (DO) and upregulated the expression of several molecular reactions, including biomarkers in endoplasmic reticulum stress (78 kDa glucose-regulated protein, GRP78 and C/EBP-homologous protein, CHOP), autophagy (Beclin-1, p62 and LC3 II) and apoptosis (caspase 3). BPAO also disturbed the Kelch-like ECH-associated protein 1-nuclear factor erythroid-2-related factor 2 (Keap1-Nrf2) pathways. These responses might collectively alter muscarinic and purinergic signaling and contribute to the presence of DO in the ischemic bladder. Therapeutically, treatment with neither a muscarinic nor purinergic receptor antagonist restored bladder function. Interestingly, sulforaphane effectively attenuated ischemia-enhanced endoplasmic reticulum stress, autophagy and apoptosis in the bladder, subsequently ameliorated ischemia-induced bladder dysfunction and might emerge as a novel strategy to protect the bladder against ischemia-induced oxidative damage.

Indexed as

IschemiaUrinary BladderUrinary Bladder, OveractiveAnimalsApoptosisAtherosclerosisAutophagyDisease Models, AnimalEndoplasmic Reticulum StressFemaleGene Expression RegulationIsothiocyanatesRatsRats, WistarSulfoxidesIsothiocyanatessulforaphaneSulfoxides

Identifiers

PMID27824068
PMCPMC5099933
OpenAlexW2551193845

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.