Evidence map›Paper›PMID 29960994›Full record

ArticleJournal of the American Heart Association2018

Discovery of an Experimental Model of Unicuspid Aortic Valve.

Robert M Weiss, Yi Chu, Robert M Brooks, Donald D Lund, Justine Cheng, Kathy A Zimmerman, Melissa K Kafa, Phanicharan Sistla, Hardik Doshi, Jian Q Shao and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of the American Heart Association, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. A novel mouse model of calcific aortic valve stenosis.Animal models and experimental medicine · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Discovery of an Experimental Model of Unicuspid Aortic Valve.Journal of the American Heart Association · 2018
    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

13 authors at 2 institutions in 1 country.

Robert M WeissDivision of Cardiovascular Medicine, Carver College of Medicine University of Iowa, Iowa City, IA robert-weiss@uiowa.edu.
Yi ChuDivision of Cardiovascular Medicine, Carver College of Medicine University of Iowa, Iowa City, IA.
Robert M BrooksDivision of Cardiovascular Medicine, Carver College of Medicine University of Iowa, Iowa City, IA.
Donald D LundDivision of Cardiovascular Medicine, Carver College of Medicine University of Iowa, Iowa City, IA.
Justine ChengDivision of Cardiovascular Medicine, Carver College of Medicine University of Iowa, Iowa City, IA.
Kathy A ZimmermanDivision of Cardiovascular Medicine, Carver College of Medicine University of Iowa, Iowa City, IA.
Melissa K KafaDivision of Cardiovascular Medicine, Carver College of Medicine University of Iowa, Iowa City, IA.
Phanicharan SistlaDivision of Cardiovascular Medicine, Carver College of Medicine University of Iowa, Iowa City, IA.
Hardik DoshiDivision of Cardiovascular Medicine, Carver College of Medicine University of Iowa, Iowa City, IA.
Jian Q ShaoThe Central Microscopy Core, Carver College of Medicine University of Iowa, Iowa City, IA.
Ramzi N El AccaouiDivision of Cardiovascular Medicine, Carver College of Medicine University of Iowa, Iowa City, IA.
Catherine M OttoDivision of Cardiology, University of Washington School of Medicine, Seattle, WA.
Donald D HeistadDivision of Cardiovascular Medicine, Carver College of Medicine University of Iowa, Iowa City, IA.
University of Iowa · USUniversity of Washington · US

Funding

High-Resolution Research UltrasoundS10OD019941 · OD · UNIVERSITY OF IOWA · PI WEISS, ROBERT M · 2015 to 2015
$298k
NIH HHS S10 OD019941
6 · The paper itself

Abstract

backgroundThe epithelial growth factor receptor family of tyrosine kinases modulates embryonic formation of semilunar valves. We hypothesized that mice heterozygous for a dominant loss-of-function mutation in epithelial growth factor receptor, which are METHODS AND

resultsAortic valves from

conclusionsA new mouse model uniquely recapitulates salient functional, structural, and histologic features of human unicuspid aortic valve disease, which are phenotypically distinct from other forms of congenital aortic valve disease. The new model may be useful for elucidating mechanisms by which congenitally anomalous aortic valves become critically dysfunctional.

Indexed as

Loss of Function MutationAnimalsAortic ValveAortic Valve InsufficiencyAortic Valve StenosisDisease Models, AnimalDisease ProgressionErbB ReceptorsFemaleGene Expression RegulationGenetic Predisposition to DiseaseHeart Defects, CongenitalHeart Valve DiseasesHemodynamicsHumansHypertrophy, Left VentricularEGFR protein, mouseErbB Receptorsaortic valveaortic valve regurgitationaortic valve stenosis

Identifiers

PMID29960994
PMCPMC6064885
OpenAlexW2810530371

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.