Evidence map›Paper›PMID 36005436›Full record

ArticleJournal of cardiovascular development and disease2022

Activation of AcvR1-Mediated Signaling Results in Semilunar Valve Defects.

Shabber Syed, Sudha Rajderkar, Jeffrey M Mann, Travis Hawkins, Bingrou Wu, Bin Zhou, Yukiko Sugi, Yuji Mishina, Vesa Kaartinen

Open access · goldAbstract read
In one paragraph

Article in Journal of cardiovascular development and disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact, top 81% 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

0 citing papers in PubMed, 0 citations in OpenAlex.

No citing paper in PubMed yet.

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

9 authors at 3 institutions in 1 country.

Shabber SyedDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI 48109, USA.
Sudha RajderkarDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI 48109, USA.ORCID 0000-0003-2001-3450
Jeffrey M MannDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI 48109, USA.
Travis HawkinsDepartment of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC 29425, USA.
Bingrou WuDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Bin ZhouDepartment of Genetics, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Yukiko SugiDepartment of Regenerative Medicine and Cell Biology, Medical University of South Carolina, Charleston, SC 29425, USA.
Yuji MishinaDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI 48109, USA.ORCID 0000-0002-6268-4204
Vesa KaartinenDepartment of Biologic and Materials Sciences, University of Michigan School of Dentistry, Ann Arbor, MI 48109, USA.ORCID 0000-0002-9432-510X
University of Michigan · USAlbert Einstein College of Medicine · USMedical University of South Carolina · US

Funding

Activin Receptor-Like Kinase-2 in Cardiac MorphogenesisR01HL074862 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAARTINEN, VESA M · 2004 to 2011
$2.6M
NHLBI NIH HHS R01 HL074862NIH HHS HL074862University of Michigan MCubed 2.0
6 · The paper itself

Abstract

Calcific aortic valve disease (CAVD) is a common cardiac defect, particularly in the aging population. While several risk factors, such as bi-leaflet valve structure and old age, have been identified in CAVD pathogenesis, molecular mechanisms resulting in this condition are still under active investigation. Bone morphogenetic protein signaling via the activin type I receptor (AcvRI) plays an important role during physiological and pathological processes involving calcification, e.g., bone formation and heterotopic ossification. In addition, AcvRI is required for normal cardiac valve development, yet its role in aortic valve disease, if any, is currently unknown. Here, we induced the expression of constitutively active AcvRI in developing mouse embryos in the endocardium and in cells at the valve leaflet-wall junction that are not of endocardium origin using the

Indexed as

calcificationTGF-beta superfamily signalingvalve defects

Identifiers

PMID36005436
PMCPMC9410128
OpenAlexW4292295109

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.