Evidence map›Paper›PMID 36414704›Full record

ArticleCommunications biology2022

Angiopoietin-like 2 is essential to aortic valve development in mice.

Pauline Labbé, Victoria Munoz Goyette, Nathalie Thorin-Trescases, Louis Villeneuve, Ines Desanlis, Constance Delwarde, Yan-Fen Shi, Cécile Martel, Carol Yu, Azadeh Alikashani and 7 more

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

8 citing papers in PubMed, 9 citations in OpenAlex.

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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

17 authors at 4 institutions in 3 countries.

Pauline LabbéMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada. pauline.labbe@icm-mhi.org.ORCID 0000-0002-1218-165X
Victoria Munoz GoyetteMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada.ORCID 0000-0003-0401-9959
Nathalie Thorin-TrescasesMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada.
Louis VilleneuveMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada.
Ines DesanlisFaculty of Medicine, Department of Medicine, Université de Montréal, Montreal Clinical Research Institute, Montreal, QC, Canada.ORCID 0000-0003-0411-717X
Constance DelwardeUniversité de Nantes, CNRS, INSERM, l'institut du thorax, Nantes, France.ORCID 0000-0002-4047-1099
Yan-Fen ShiMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada.
Cécile MartelMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada.
Carol YuMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada.
Azadeh AlikashaniMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada.
Maya MamarbachiMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada.
Frédéric LesageMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada.
Samuel MathieuFaculty of Medicine, Department of Surgery, Université Laval, Quebec, QC, Canada.
Jean-Claude TardifMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada.ORCID 0000-0002-8200-8983
Patrick MathieuFaculty of Medicine, Department of Surgery, Université Laval, Quebec, QC, Canada.ORCID 0000-0002-3805-2004
Marie KmitaFaculty of Medicine, Department of Medicine, Université de Montréal, Montreal Clinical Research Institute, Montreal, QC, Canada.ORCID 0000-0003-4021-0478
Éric ThorinMontreal Heart Institute, Université de Montréal, Montreal, QC, Canada.ORCID 0000-0001-5827-8935
Montreal Heart Institute · CAMontreal Clinical Research Institute · CAUniversité Laval · CACentre National de la Recherche Scientifique · FR

Funding

CIHR 162446CIHR 166110
6 · The paper itself

Abstract

Aortic valve (AoV) abnormalities during embryogenesis are a major risk for the development of aortic valve stenosis (AVS) and cardiac events later in life. Here, we identify an unexpected role for Angiopoietin-like 2 (ANGPTL2), a pro-inflammatory protein secreted by senescent cells, in valvulogenesis. At late embryonic stage, mice knocked-down for Angptl2 (Angptl2-KD) exhibit a premature thickening of AoV leaflets associated with a dysregulation of the fine balance between cell apoptosis, senescence and proliferation during AoV remodeling and a decrease in the crucial Notch signalling. These structural and molecular abnormalities lead toward spontaneous AVS with elevated trans-aortic gradient in adult mice of both sexes. Consistently, ANGPTL2 expression is detected in human fetal semilunar valves and associated with pathways involved in cell cycle and senescence. Altogether, these findings suggest that Angptl2 is essential for valvulogenesis, and identify Angptl2-KD mice as an animal model to study spontaneous AVS, a disease with unmet medical need.

Indexed as

Angiopoietin-Like Protein 2Aortic ValveAortic Valve StenosisAnimalsDisease Models, AnimalFemaleHumansMaleMiceSignal TransductionAngiopoietin-Like Protein 2ANGPTL2 protein, humanAngptl2 protein, mouse

Identifiers

PMID36414704
PMCPMC9681843
OpenAlexW4309650920

What Socratic 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 Socratic graph.