Evidence map›Paper›PMID 27122250›Full record

ArticleScientific reports2016

Interaction of Caveolin-3 and HCN is involved in the pathogenesis of diabetic cystopathy.

Xingyou Dong, Qixiang Song, Jingzhen Zhu, Jiang Zhao, Qian Liu, Teng Zhang, Zhou Long, Jia Li, Chao Wu, Qingqing Wang and 3 more

Abstract read
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. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. HCN as a Mediator of Urinary Homeostasis: Age-Associated Changes in Expression and Function in Adrenergic Detrusor Relaxation.The journals of gerontology. Series A, Biological sciences and medical sciences · 2019
    Article
  9. Article
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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

13 authors.

Xingyou DongDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Qixiang SongDepartment of Biomedical Engineering, the Cleveland Clinic, Cleveland, OH, United States of America.
Jingzhen ZhuDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Jiang ZhaoDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Qian LiuDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Teng ZhangDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Zhou LongDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Jia LiDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Chao WuDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Qingqing WangDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Xiaoyan HuDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.
Margot DamaserDepartment of Biomedical Engineering, the Cleveland Clinic, Cleveland, OH, United States of America.
Longkun LiDepartment of Urology, Second Affiliated Hospital, Third Military Medical University, Chongqing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A growing body of research suggests that impaired bladder Cajal-like interstitial cells (ICCs) are a important component in the pathogenesis of diabetes-induced bladder dysfunction, although the molecular mechanisms have not been illustrated completely. The purpose of this study was to examine whether the hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in ICCs-DM were responsible for the detrusor weak contractility of Diabetic cystopathy (DCP) and to study the possible mechanism of regulating the expression and function of HCN channels. HCN channels expression were decreased at the mRNA and protein levels. Forskolin (FSK), which can elevate intracellular cAMP levels, increased the density of the hyperpolarization-activated current and intracellular calcium concentration in both normal control (NC) rats and DCP rats, but the sensitivity of FSK on HCN channels was clearly down-regulated in DCP rats. The loss of caveolae and caveolin was in accordance with the decrease in HCN channels. Caveolin-3 co-localizes with and affects the expression and function of HCN. Taken together, these results indicate that the loss of caveolae and HCN channels in ICCs-DM is important in the pathogenesis of DCP. Increasing the number of caveolae to enhance the function of HCN channels may represent a viable target for the pharmacological treatment of DCP.

Indexed as

AnimalsCaveolin 3Diabetes ComplicationsGene Expression ProfilingHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsPotassium ChannelsRatsRNA, MessengerUrinary Bladder DiseasesCaveolin 3Hcn1 protein, ratHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsPotassium ChannelsRNA, Messenger

Identifiers

PMID27122250
PMCPMC4848475

What OpenQuestion holds

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LicenceCC BY
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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.