Evidence map›Paper›PMID 24123312›Full record

ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2014

Epicardial-derived adrenomedullin drives cardiac hyperplasia during embryogenesis.

Sarah E Wetzel-Strong, Manyu Li, Klara R Klein, Toshio Nishikimi, Kathleen M Caron

Open access · bronzeAbstract read
In one paragraph

Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.3field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

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  12. CXCR7 Targeting and Its Major Disease Relevance.Frontiers in pharmacology · 2018
    Review
  13. Article
  14. Cohort of estrogen-induced microRNAs regulate adrenomedullin expression.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  15. Adrenomedullin in lymphangiogenesis: from development to disease.Cellular and molecular life sciences : CMLS · 2015
    Review
  16. Article
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  18. Review
  19. Article
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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

5 authors at 2 institutions in 2 countries.

Sarah E Wetzel-Strong
Manyu Li
Klara R Klein
Toshio Nishikimi
Kathleen M Caron
University of North Carolina at Chapel Hill · USKyoto University · JP

Funding

Pre-doctoral Training Program in Integrative Vascular BiologyT32HL069768 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Christopher P. Mack · 2002 to 2026
$9.7M
Adrenomedullin Signaling at the Maternal-Fetal InterfaceR01HD060860 · NICHD · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Kathleen M Caron · 2009 to 2026
$4.8M
Adrenomedullin Signaling in Vascular DevelopmentR01HL091973 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CARON, KATHLEEN M · 2008 to 2011
$1.4M
Decoy Receptors in LymphangiogenesisF30HL118932 · NHLBI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI KLEIN, KLARA RACHEL · 2013 to 2016
$149k
NHLBI NIH HHS F30 HL118932NHLBI NIH HHS HL091973NHLBI NIH HHS R01 HL091973NHLBI NIH HHS T32 HL069768NICHD NIH HHS HD060860NICHD NIH HHS R01 HD060860
6 · The paper itself

Abstract

backgroundGrowth promoting signals from the epicardium are essential for driving myocardial proliferation during embryogenesis. In adults, these signals become reactivated following injury and promote angiogenesis and myocardial repair. Therefore, identification of such paracrine factors could lead to novel therapeutic strategies. The multi-functional peptide adrenomedullin (Adm 5 gene, AM 5 protein) is required for normal heart development. Moreover, elevated plasma AM following myocardial infarction offers beneficial cardioprotection and serves as a powerful diagnostic and prognostic indication of disease severity.

resultsHere, we developed a new model of Adm overexpression by stabilizing the Adm mRNA through gene-targeted replacement of the endogenous 30 untranslated region. As expected, Admhi/hi mice express three-times more AM than controls in multiple tissues, including the heart. Despite normal blood pressures, Admhi/hi mice unexpectedly showed significantly enlarged hearts due to increased cardiac hyperplasia during development. The targeting vector was designed to allow for reversion to wild-type levels by means of Cre-mediated modification. Using this approach, we demonstrate that AM derived from the epicardium, but not the myocardium or cardiac fibroblast, is responsible for driving cardiomyocyte hyperplasia.

conclusionsAM is produced by the epicardium and drives myocyte proliferation during development, thus representing a novel and clinically relevant factor potentially related to mechanisms of cardiac repair after injury.

Indexed as

AdrenomedullinAnimalsBlotting, WesternBromodeoxyuridineCell CycleDNA PrimersGenetic VectorsHeartHyperplasiaMiceMice, Mutant StrainsMyocardiumMyocytes, CardiacPericardiumReal-Time Polymerase Chain ReactionRNA StabilityAdrenomedullinBromodeoxyuridineDNA Primers

Identifiers

PMID24123312
PMCPMC4009724
OpenAlexW1788141947

What OpenQuestion holds

Textmetadata
LicenceTDM
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.