Evidence map›Paper›PMID 20116383›Full record

ArticleJournal of molecular and cellular cardiology2010

The influence of FGF2 high molecular weight (HMW) isoforms in the development of cardiac ischemia-reperfusion injury.

Siyun Liao, Janet R Bodmer, Mohamad Azhar, Gilbert Newman, J Douglas Coffin, Thomas Doetschman, Jo El J Schultz

Abstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 29% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 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

7 authors at 3 institutions in 1 country.

Siyun LiaoDepartment of Pharmacology and Cell Biophysics, University of Cincinnati, College of Medicine, 231 Albert Sabin Way, ML 0575, Cincinnati, OH 45267, USA.
Janet R Bodmer
Mohamad Azhar
Gilbert Newman
J Douglas Coffin
Thomas Doetschman
Jo El J Schultz
Sabin Vaccine Institute · USUniversity of Cincinnati Medical Center · USUniversity of Montana · US

Funding

Signaling Mechanisms of FGF2-induced CardioprotectionR01HL075633 · NHLBI · UNIVERSITY OF CINCINNATI · PI SCHULTZ, JOEL J · 2004 to 2014
$3.5M
TARGETED MUTATION OF TGF-BETA-1 IN ES CELLSR01HD026471 · NICHD · UNIVERSITY OF CINCINNATI · PI DOETSCHMAN, THOMAS · 1990 to 2005
$1.8M
Roles of FGF2 and TGFbeta in cardiac hypertrophyR01HL070174 · NHLBI · UNIVERSITY OF CINCINNATI · PI DOETSCHMAN, THOMAS · 2002 to 2005
$1.5M
Signaling Mechanisms of FGF2-induced CardioprotectionR56HL075633 · NHLBI · UNIVERSITY OF CINCINNATI · PI SCHULTZ, JOEL J · 2009 to 2009
$393k
NHLBI NIH HHS R01 HL070174NHLBI NIH HHS R01 HL075633NHLBI NIH HHS R56 HL075633NICHD NIH HHS R01 HD026471
6 · The paper itself

Abstract

Fibroblast growth factor 2 (FGF2) consists of multiple protein isoforms (low [LMW] and high molecular weight [HMW]), which are localized to different cellular compartments, indicating unique biological activity. We previously showed that the LMW isoform is important in protecting the heart from myocardial dysfunction associated with ischemia-reperfusion (I/R) injury, but the roles of the HMW isoforms remain unknown. To elucidate the role of HMW isoforms in I/R and cardioprotection, hearts from novel mouse models, in which the murine FGF2 HMWs are knocked out (HMWKO) or the human FGF2 24 kDa HMW isoform is overexpressed (HMW Tg) and their wildtype (Wt) or non-transgenic (NTg) cohorts were subjected to an ex vivo work-performing heart model of I/R. There was a significant improvement in post-ischemic recovery of cardiac function in HMWKO hearts (76+/-5%, p<0.05) compared to Wt hearts (55+/-5%), with a corresponding decrease in HMW Tg function (line 20: 38+/-6% and line 28: 33+/-4%, p<0.05) compared to non-transgenic hearts (68+/-9%). FGF2 LMW isoform was secreted from Wt and HMWKO hearts during I/R, and a FGF receptor (FGFR) inhibitor, PD173074 caused a decrease in cardiac function when administered in I/R in Wt and FGF2 HMWKO hearts (p<0.05), indicating that FGFR is involved in FGF2 LMW isoform's biological effect in ischemia-reperfusion injury. Moreover, overexpression of HMW isoform reduced FGFR1 phosphorylation/activation with no further decrease in the phosphorylation state in the presence of the FGFR inhibitor. Overall, our data indicate that HMW isoforms have a detrimental role in the development of post-ischemic myocardial dysfunction.

Indexed as

AnimalsCreatine KinaseFibroblast Growth Factor 2HeartHumansMiceMice, KnockoutMice, TransgenicMolecular WeightMyocardial Reperfusion InjuryMyocardiumPhosphorylationProtein IsoformsReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 4Reperfusion InjuryCreatine KinaseFgfr1 protein, mouseFgfr4 protein, mouseFibroblast Growth Factor 2Protein IsoformsReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 4

Identifiers

PMID20116383
PMCPMC3842106
OpenAlexW2000832385

What OpenQuestion holds

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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.