Evidence map›Paper›PMID 21324930›Full record

ArticleDisease models & mechanisms2011

Experimental myocardial infarction triggers canonical Wnt signaling and endothelial-to-mesenchymal transition.

Omonigho Aisagbonhi, Meena Rai, Sergey Ryzhov, Nick Atria, Igor Feoktistov, Antonis K Hatzopoulos

Registry-linked trialOpen access · goldAbstract read
In one paragraph

Article in Disease models & mechanisms, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03342131 (Change of Serum Wnt2 or Wnt4 and the Relationship With Hs-CRP,cTnI and Prognosis in Patients With Acute Coronary Syndrome), which is not on this map. Cited by 185 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
185citing papers in PubMed, 2 pooled it
8.4field-weighted citation impact, top 2% 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.

NCT03342131 unknown statusnot on this mapstarted 2017, after this paper: background citation

Change of Serum Wnt2 or Wnt4 and the Relationship With Hs-CRP,cTnI and Prognosis in Patients With Acute Coronary Syndrome

TypeobservationalSponsorThe First Affiliated Hospital of Dalian Medical UniversityRan2017 to 2019Enrolled450ConditionsAcute Coronary SyndromeArmsCirculating wnt 2 and wnt 4 concentration
3 · Its place in the literature

Who cites it

185 citing papers in PubMed, 2 syntheses or guidelines pooled it, 297 citations in OpenAlex.

  1. Pooled it
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  12. Endothelial to mesenchymal transition: a central mechanism in diabetes-induced vascular pathology.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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125 more citing papers are in PubMed but not listed here.

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

6 authors at 1 institution in 1 country.

Omonigho AisagbonhiDepartment of Medicine, Division of Cardiovascular Medicine, Vanderbilt University, 2213 Garland Avenue, Nashville, TN 37232-6300, USA.
Meena Rai
Sergey Ryzhov
Nick Atria
Igor Feoktistov
Antonis K Hatzopoulos
Vanderbilt University · US

Funding

MEDICAL SCIENTIST TRAINING PROGRAMT32GM007347 · NIGMS · VANDERBILT UNIVERSITY · PI WILLIAMS, CHRISTOPHER S. · 1985 to 2023
$26.3M
Optimizing Cardiovascular Stem Cells for Cardiac Repair and RegenerationU01HL100398 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI HATZOPOULOS, ANTONIS · 2009 to 2015
$8.0M
Wnt-Pathway Modulators in Cardioprotection after IschemiR01HL083958 · NHLBI · VANDERBILT UNIVERSITY · PI HATZOPOULOS, ANTONIS · 2006 to 2010
$2.2M
Role of Adenosine Receptors in NeovascularizationR01HL095787 · NHLBI · VANDERBILT UNIVERSITY · PI FEOKTISTOV, IGOR · 2010 to 2013
$1.5M
NHLBI NIH HHS HL083958NHLBI NIH HHS HL100398NHLBI NIH HHS R01 HL083958NHLBI NIH HHS R01 HL095787NHLBI NIH HHS U01 HL100398NIGMS NIH HHS T32 GM007347NIGMS NIH HHS T32GM07347
6 · The paper itself

Abstract

Despite available therapies, myocardial infarction (MI) remains a leading cause of death worldwide. Better understanding of the molecular and cellular mechanisms that regulate cardiac repair should help to improve the clinical outcome of MI patients. Using the reporter mouse line TOPGAL, we show that canonical (β-catenin-dependent) Wnt signaling is induced 4 days after experimental MI in subepicardial endothelial cells and perivascular smooth muscle actin (SMA)-positive (SMA(+)) cells. At 1 week after ischemic injury, a large number of canonical-Wnt-positive cells accumulated in the infarct area during granulation tissue formation. Coincidently with canonical Wnt activation, endothelial-to-mesenchymal transition (EndMT) was also triggered after MI. Using cell lineage tracing, we show that a significant portion of the canonical-Wnt-marked SMA(+) mesenchymal cells is derived from endothelial cells. Canonical Wnt signaling induces mesenchymal characteristics in cultured endothelial cells, suggesting a direct role in EndMT. In conclusion, our study demonstrates that canonical Wnt activation and EndMT are molecular and cellular responses to MI and that canonical Wnt signaling activity is a characteristic property of EndMT-derived mesenchymal cells that take part in cardiac tissue repair after MI. These findings could lead to new strategies to improve the course of cardiac repair by temporal and cell-type-specific manipulation of canonical Wnt signaling.

Indexed as

Signal TransductionActinsAnimalsBlood VesselsCells, CulturedEndothelial CellsEndotheliumGranulation TissueHeart ValvesIntercellular Signaling Peptides and ProteinsMesodermMiceModels, BiologicalMyocardial InfarctionMyocardiumMyofibroblastsActinsalpha-smooth muscle actin, mouseIntercellular Signaling Peptides and ProteinsWnt Proteins

Identifiers

PMID21324930
PMCPMC3124051
OpenAlexW2051075947

What OpenQuestion holds

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LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

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.