Evidence map›Paper›PMID 27921040›Full record

ReviewKidney diseases (Basel, Switzerland)2016

New Insights into the Molecular Mechanisms Targeting Tubular Channels/Transporters in PKD Development.

Ming Wu, Shengqiang Yu

Open access · goldAbstract readReview
In one paragraph

Review in Kidney diseases (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.9field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. The Biology of Vasopressin.Biomedicines · 2021
    Review
  5. Review
  6. Article
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

2 authors at 1 institution in 1 country.

Ming WuKidney Institute of PLA, Division of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, PR China.
Shengqiang YuKidney Institute of PLA, Division of Nephrology, Shanghai Changzheng Hospital, Second Military Medical University, Shanghai, PR China.
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutosomal dominant polycystic kidney disease (PKD) or autosomal recessive PKD is caused by a mutation in the SUMMARY: Polycystin-2 by itself is a calcium-permeable cation channel, and its channel function can be regulated by polycystin-1 or fibrocystin. In this paper, we reviewed the current knowledge about calcium transports and cyclic adenosine monophosphate (cAMP)-driven chloride transports in PKD. In addition, the function and the underlining mechanism of glucose transporters, phosphate transporters and water channels in PKD are also discussed. KEY MESSAGES: Abnormalities in calcium handling and exuberant cAMP-dependent cystic fibrosis transmembrane conductance regulator-mediated fluid secretion in the collecting duct are the most important issues in the pathogenesis of PKD.

Indexed as

ChannelsMolecular mechanismPolycystic kidney diseaseTransporters

Identifiers

PMID27921040
PMCPMC5123004
OpenAlexW2326755960

What OpenQuestion holds

Textmetadata
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.