Evidence map›Paper›PMID 34445719›Full record

ArticleInternational journal of molecular sciences2021

Zebrafish Model as a Screen to Prevent Cyst Inflation in Autosomal Dominant Polycystic Kidney Disease.

Inês Oliveira, Raquel Jacinto, Sara Pestana, Fernando Nolasco, Joaquim Calado, Susana Santos Lopes, Mónica Roxo-Rosa

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed, 1 pooled it
0.2field-weighted citation impact, top 39% 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

3 citing papers in PubMed, 1 synthesis or guideline pooled it, 3 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
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

7 authors at 2 institutions in 1 country.

Inês OliveiraCEDOC, Chronic Diseases Research Center, NOVA Medical School|Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Campo Mártires da Pátria, 130, 1169-056 Lisboa, Portugal.
Raquel JacintoCEDOC, Chronic Diseases Research Center, NOVA Medical School|Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Campo Mártires da Pátria, 130, 1169-056 Lisboa, Portugal.ORCID 0000-0002-4029-0204
Sara PestanaCEDOC, Chronic Diseases Research Center, NOVA Medical School|Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Campo Mártires da Pátria, 130, 1169-056 Lisboa, Portugal.
Fernando NolascoDepartment of Nephrology, Centro Hospitalar e Universitário de Lisboa Central, Hospital de Curry Cabral, Rua da Beneficência, 8, 1069-166 Lisboa, Portugal.
Joaquim CaladoDepartment of Nephrology, Centro Hospitalar e Universitário de Lisboa Central, Hospital de Curry Cabral, Rua da Beneficência, 8, 1069-166 Lisboa, Portugal.
Susana Santos LopesCEDOC, Chronic Diseases Research Center, NOVA Medical School|Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Campo Mártires da Pátria, 130, 1169-056 Lisboa, Portugal.
Mónica Roxo-RosaCEDOC, Chronic Diseases Research Center, NOVA Medical School|Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Campo Mártires da Pátria, 130, 1169-056 Lisboa, Portugal.
Universidade Nova de Lisboa · PTHospital Curry Cabral · PT

Funding

Fundação para a Ciência e a Tecnologia FCT-ANR/BEX-BID/0153/2012Fundação para a Ciência e a Tecnologia iNOVA4Health-UID/Multi/04462/2013Fundação para a Ciência e a Tecnologia LISBOA-01-0145-FEDER-022170Fundação para a Ciência e a Tecnologia PTDC/BEX-BID/1411/2014Horizon 2020 811087Sociedade Portuguesa de Nefrologia Projecto de 2015
6 · The paper itself

Abstract

In autosomal dominant polycystic kidney disease (ADPKD), kidney cyst growth requires the recruitment of CFTR (cystic fibrosis transmembrane conductance regulator), the chloride channel that is defective in cystic fibrosis. We have been studying cyst inflation using the zebrafish Kupffer's vesicle (KV) as model system because we previously demonstrated that knocking down polycystin 2 (PC2) induced a CFTR-mediated enlargement of the organ. We have now quantified the PC2 knockdown by showing that it causes a 73% reduction in the number of KV cilia expressing PC2. According to the literature, this is an essential event in kidney cystogenesis in ADPKD mice. Additionally, we demonstrated that the PC2 knockdown leads to a significant accumulation of CFTR-GFP at the apical region of the KV cells. Furthermore, we determined that KV enlargement is rescued by the injection of Xenopus

Indexed as

AnimalsCiliaCystic Fibrosis Transmembrane Conductance RegulatorCystsDisease Models, AnimalKidneyKupffer CellsPolycystic Kidney, Autosomal DominantTRPP Cation ChannelsZebrafishZebrafish ProteinsCFTR protein, zebrafishCystic Fibrosis Transmembrane Conductance RegulatorTRPP Cation ChannelsZebrafish Proteinsautosomal dominant polycystic kidney disease (ADPKD)cystic fibrosis transmembrane conductance regulator (CFTR)Kupffer’s vesicle (KV)polycystin-2 (PC2)

Identifiers

PMID34445719
PMCPMC8396643
OpenAlexW3193622827

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.