Evidence map›Paper›PMID 21849352›Full record

ArticleEuropean heart journal2012

Granulocyte colony-stimulating factor treatment plus dipeptidylpeptidase-IV inhibition augments myocardial regeneration in mice expressing cyclin D2 in adult cardiomyocytes.

Marc-Michael Zaruba, Wuqiang Zhu, Mark H Soonpaa, Sean Reuter, Wolfgang-Michael Franz, Loren J Field

Open access · bronzeAbstract read
In one paragraph

Article in European heart journal, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.3field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

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  12. VEGF nanoparticles repair the heart after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2018
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  20. Glucagon-like peptide-1 and its cardiovascular effects.Current atherosclerosis reports · 2012
    Review
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 3 institutions in 2 countries.

Marc-Michael ZarubaMedical Department I, Klinikum Grossh, Ludwig-Maximilians University, Marchioninistrasse 15, Munich 81377, Germany. marc-michael.zaruba@med.uni-muenchen.de
Wuqiang Zhu
Mark H Soonpaa
Sean Reuter
Wolfgang-Michael Franz
Loren J Field
Indiana University – Purdue University Indianapolis · USIndiana University School of MedicineLudwig-Maximilians-Universität München · DE

Funding

REGULATION OF CARDIOMYOCYTE SURVIVALP01HL085098 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIELD, LOREN J · 2007 to 2011
$10.9M
Genetic Enhancement of Cardiac Repair with Adult Stem CellsR01HL083126 · NHLBI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI FIELD, LOREN J · 2006 to 2015
$2.9M
Cell cycle activation for cardiac repairR01HL109205 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI FIELD, LOREN J · 2011 to 2015
$1.9M
NHLBI NIH HHS HL083126NHLBI NIH HHS HL085098NHLBI NIH HHS R01 HL083126NHLBI NIH HHS R01 HL109205
6 · The paper itself

Abstract

aimsAlthough pharmacological interventions that mobilize stem cells and enhance their homing to damaged tissue can limit adverse post-myocardial infarction (MI) remodelling, cardiomyocyte renewal with this approach is limited. While experimental cell cycle induction can promote cardiomyocyte renewal following MI, this process must compete with the more rapid processes of scar formation and adverse remodelling. The current study tested the hypothesis that the combination of enhanced stem cell mobilization/homing and cardiomyocyte cell cycle induction would result in increased myocardial renewal in injured hearts. METHODS AND

resultsMyocardial infarction was induced by coronary artery ligation in adult MHC-cycD2 transgenic mice (which exhibit constitutive cardiomyocyte cell cycle activity) and their non-transgenic littermates. Mice were then treated with saline or with granulocyte colony-stimulating factor (G-CSF) plus the dipeptidylpeptidase-IV (DPP-IV) inhibitor Diprotin A (DipA) for 7 days. Infarct thickness and cardiomyocyte number/infarct/section were significantly improved in MHC-cycD2 mice with G-CSF plus DipA treatment when compared with MHC-cycD2 transgene expression or G-CSF plus DipA treatment alone. Echocardiographic analyses revealed that stem cell mobilization/homing and cardiomyocyte cell cycle activation had an additive effect on functional recovery.

conclusionThese data strongly suggest that G-CSF plus DPP-IV inhibition, combined with cardiomyocyte cell cycle activation, leads to enhanced myocardial regeneration following MI. The data are also consistent with the notion that altering adverse post-injury remodelling renders the myocardium more permissive for cardiomyocyte repopulation.

Indexed as

AnimalsCyclin D2Dipeptidyl-Peptidase IV InhibitorsDrug CombinationsGranulocyte Colony-Stimulating FactorHeartHematopoietic Stem Cell MobilizationMiceMice, TransgenicMyocardial InfarctionMyocytes, CardiacRandom AllocationRegenerationStroke VolumeCyclin D2Dipeptidyl-Peptidase IV InhibitorsDrug CombinationsGranulocyte Colony-Stimulating Factor

Identifiers

PMID21849352
PMCPMC3249220
OpenAlexW2166240885

What OpenQuestion holds

Textmetadata
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.