Evidence map›Paper›PMID 30847422›Full record

ArticleJACC. Basic to translational science2019

Connective Tissue Growth Factor Inhibition Enhances Cardiac Repair and Limits Fibrosis After Myocardial Infarction.

Laura E Vainio, Zoltán Szabó, Ruizhu Lin, Johanna Ulvila, Raisa Yrjölä, Tarja Alakoski, Jarkko Piuhola, Walter J Koch, Heikki Ruskoaho, Shaun D Fouse and 6 more

Open access · goldAbstract read
In one paragraph

Article in JACC. Basic to translational science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

45 citing papers in PubMed, 72 citations in OpenAlex.

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  15. CHI3L1 promotes myocardial fibrosis via regulating lncRNA TUG1/miR-495-3p/ETS1 axis.Apoptosis : an international journal on programmed cell death · 2023
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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

16 authors at 4 institutions in 2 countries.

Laura E VainioResearch Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland.
Zoltán SzabóResearch Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland.
Ruizhu LinResearch Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland.
Johanna UlvilaResearch Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland.
Raisa YrjöläResearch Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland.
Tarja AlakoskiResearch Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland.
Jarkko PiuholaDivision of Cardiology, Department of Internal Medicine, Oulu University Hospital and University of Oulu, Oulu, Finland.
Walter J KochCenter for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania.
Heikki RuskoahoDivision of Pharmacology and Pharmacotherapy, Faculty of Pharmacy, University of Helsinki, Helsinki, Finland.
Shaun D FouseFibroGen, Inc., San Francisco, California.
Todd W SeeleyFibroGen, Inc., San Francisco, California.
Erhe GaoCenter for Translational Medicine, Lewis Katz School of Medicine, Temple University, Philadelphia, Pennsylvania.
Pierre SignoreFibroGen, Inc., San Francisco, California.
Kenneth E LipsonFibroGen, Inc., San Francisco, California.
Johanna MaggaResearch Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland.
Risto KerkeläResearch Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland.
University of Oulu · FIFibroGen (United States) · USTemple University · USUniversity of Helsinki · FI

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction (MI)-induced cardiac fibrosis attenuates cardiac contractile function, and predisposes to arrhythmias and sudden cardiac death. Expression of connective tissue growth factor (CTGF) is elevated in affected organs in virtually every fibrotic disorder and in the diseased human myocardium. Mice were subjected to treatment with a CTGF monoclonal antibody (mAb) during infarct repair, post-MI left ventricular (LV) remodeling, or acute ischemia-reperfusion injury. CTGF mAb therapy during infarct repair improved survival and reduced LV dysfunction, and reduced post-MI LV hypertrophy and fibrosis. Mechanistically, CTGF mAb therapy induced expression of cardiac developmental and/or repair genes and attenuated expression of inflammatory and/or fibrotic genes.

Indexed as

connective tissue growth factor monoclonal antibodyCTGF, connective tissue growth factorECM, extracellular matrixERK, extracellular signal-regulated kinaseFB, fibroblastfibrosisheart failureHF, heart failureIg, immunoglobulinI/R, ischemia−reperfusionischemia−reperfusion injuryJNK, c-Jun N-terminal kinaseleft ventricleLV, left ventricularmAb, monoclonal antibodyMI, myocardial infarctionmyocardial infarctionTGF, transforming growth factor

Identifiers

PMID30847422
PMCPMC6390503
OpenAlexW2916723837

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.