Evidence map›Paper›PMID 34072818›Full record

ArticleInternational journal of molecular sciences2021

Smooth Muscle Specific Ablation of CXCL12 in Mice Downregulates CXCR7 Associated with Defective Coronary Arteries and Cardiac Hypertrophy.

Santhosh Kumar Ghadge, Moritz Messner, Herbert Seiringer, Thomas Maurer, Simon Staggl, Tanja Zeller, Christian Müller, Daniela Börnigen, Wolfgang J Weninger, Stefan H Geyer and 5 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.3field-weighted citation impact, top 17% 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

7 citing papers in PubMed, 16 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

15 authors at 3 institutions in 2 countries.

Santhosh Kumar GhadgeDepartment of Internal Medicine III, Cardiology and Angiology, Medical University Innsbruck, 6020 Innsbruck, Austria.
Moritz MessnerDepartment of Internal Medicine III, Cardiology and Angiology, Medical University Innsbruck, 6020 Innsbruck, Austria.
Herbert SeiringerDepartment of Internal Medicine III, Cardiology and Angiology, Medical University Innsbruck, 6020 Innsbruck, Austria.
Thomas MaurerDepartment of Internal Medicine III, Cardiology and Angiology, Medical University Innsbruck, 6020 Innsbruck, Austria.
Simon StagglDepartment of Internal Medicine III, Cardiology and Angiology, Medical University Innsbruck, 6020 Innsbruck, Austria.
Tanja ZellerClinic for Cardiology, Medical University Center Hamburg-Eppendorf, University Heart and Vascular Center Hamburg, 20251 Hamburg, Germany.
Christian MüllerClinic for Cardiology, Medical University Center Hamburg-Eppendorf, University Heart and Vascular Center Hamburg, 20251 Hamburg, Germany.
Daniela BörnigenClinic for Cardiology, Medical University Center Hamburg-Eppendorf, University Heart and Vascular Center Hamburg, 20251 Hamburg, Germany.
Wolfgang J WeningerDivision of Anatomy & MIC, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-0575-0073
Stefan H GeyerDivision of Anatomy & MIC, Medical University of Vienna, 1090 Vienna, Austria.ORCID 0000-0003-2283-4439
Sieghart SopperDepartment of Internal Medicine V, Hematology and Oncology, Medical University Innsbruck, 6020 Innsbruck, Austria.ORCID 0000-0003-2265-1974
Anne KrogsdamDivision of Bioinformatics, Medical University Innsbruck, Biocenter, 6020 Innsbruck, Austria.
Gerhard PölzlDepartment of Internal Medicine III, Cardiology and Angiology, Medical University Innsbruck, 6020 Innsbruck, Austria.
Axel BauerDepartment of Internal Medicine III, Cardiology and Angiology, Medical University Innsbruck, 6020 Innsbruck, Austria.
Marc-Michael ZarubaDepartment of Internal Medicine III, Cardiology and Angiology, Medical University Innsbruck, 6020 Innsbruck, Austria.ORCID 0000-0003-1074-5463
Innsbruck Medical University · ATUniversität Hamburg · DEMedical University of Vienna · AT

Funding

Austrian Science Fund FWF P 28817-B28Austrian Science Fund FWF P 28817Österreichische Forschungsförderungsgesellschaft Grant 858057
6 · The paper itself

Abstract

The chemokine CXCL12 plays a fundamental role in cardiovascular development, cell trafficking, and myocardial repair. Human genome-wide association studies even have identified novel loci downstream of the CXCL12 gene locus associated with coronary artery disease and myocardial infarction. Nevertheless, cell and tissue specific effects of CXCL12 are barely understood. Since we detected high expression of CXCL12 in smooth muscle (SM) cells, we generated a SM22-alpha-Cre driven mouse model to ablate CXCL12 (SM-CXCL12

Indexed as

Ablation TechniquesAnimalsCardiomegalyChemokine CXCL12Coronary VesselsDisease Models, AnimalGene Expression RegulationHumansMacrophagesMiceMuscle, SmoothMyocardial InfarctionMyocardiumReceptors, CXCRChemokine CXCL12Cmkor1 protein, mouseCxcl12 protein, mouseReceptors, CXCRcardiac hypertrophycoronary arteryCXCL12fibrosisM2 macrophagesremodelingsmooth muscle cells

Identifiers

PMID34072818
PMCPMC8198701
OpenAlexW3165687519

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.