Evidence map›Paper›PMID 28157139›Full record

ArticleCurrent opinion in cardiology2017

Genetic basis of aortic valvular disease.

Sara N Koenig, Joy Lincoln, Vidu Garg

Open access · greenAbstract read
In one paragraph

Article in Current opinion in cardiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
3.0field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Clinical Use of Blood Flow Analysis through 4D-Flow Imaging in Aortic Valve Disease.Journal of cardiovascular development and disease · 2023
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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

3 authors at 2 institutions in 2 countries.

Sara N KoenigaCenter for Cardiovascular Research bThe Heart Center, Nationwide Children's Hospital cBiomedical Sciences Graduate Program dDepartment of Pediatrics eDepartment of Molecular Genetics, Ohio State University, Columbus, Ohio, USA.
Joy Lincoln
Vidu Garg
Nationwide Children's Hospital · USInstitute of Biomedical Science · GB

Funding

Exome sequencing and functional studies in familial CHDR01HL109758 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GARG, VIDU, MCBRIDE, KIM LEWIS · 2012 to 2015
$2.7M
The Role of Notch in Calcific Aortic Valve DiseaseR01HL132801 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GARG, VIDU, LILLY, BRENDA J · 2016 to 2019
$2.6M
Molecular Mechanisms of Aortic Valve FormationR01HL121797 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI GARG, VIDU · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL109758NHLBI NIH HHS R01 HL121797NHLBI NIH HHS R01 HL132801
6 · The paper itself

Abstract

purpose of reviewAortic valve disease is relatively common and encompasses both congenital and acquired forms. Bicuspid aortic valve (BAV) is the most common type of cardiac malformation and predisposes to the development of calcific aortic valve disease (CAVD). Since the description of the link between NOTCH1, BAV and CAVD approximately a decade ago, there have been significant advances in the genetic and molecular understanding of these diseases. RECENT

findingsRecent work has defined the congenital cardiac phenotypes linked to mutations in NOTCH1, and in addition, novel etiologic genes for BAV have been discovered using new genetic technologies in humans. Furthermore, several mouse models of BAV have been described defining the role of endothelial Notch1 in aortic valve morphogenesis, whereas others have implicated new genes. These murine models along with other cell-based studies have led to molecular insights in the pathogenesis of CAVD. SUMMARY: These findings provide important insights into the molecular and genetic basis of aortic valve malformations, including BAV, specifically highlighting the etiologic role of endothelial cells. In addition, numerous investigations in to the mechanisms of CAVD demonstrate the importance of developmental origins and signaling pathways as well as communication between valve endothelial cells and the underlying interstitial cells in valve disease onset and progression.

Identifiers

PMID28157139
PMCPMC5783785
OpenAlexW2588385730

What OpenQuestion holds

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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.