Evidence map›Paper›PMID 21441138›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2011

Disrupting the EMMPRIN (CD147)-cyclophilin A interaction reduces infarct size and preserves systolic function after myocardial ischemia and reperfusion.

Peter Seizer, Carmen Ochmann, Tanja Schönberger, Sebastian Zach, Melanie Rose, Oliver Borst, Karin Klingel, Reinhard Kandolf, H Robson MacDonald, Romana A Nowak and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

52 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
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  4. Review
  5. Article
  6. Non-Immunosuppressive Cyclophilin Inhibitors.Angewandte Chemie (International ed. in English) · 2022
    Review
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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

14 authors at 2 institutions in 1 country.

Peter SeizerMedizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, Germany.
Carmen Ochmann
Tanja Schönberger
Sebastian Zach
Melanie Rose
Oliver Borst
Karin Klingel
Reinhard Kandolf
H Robson MacDonald
Romana A Nowak
Stefan Engelhardt
Florian Lang
Meinrad Gawaz
Andreas E May
University of Illinois Urbana-Champaign · USUrbana University · US

Funding

Tissue Procurement and Cell CultureU54HD040093 · NICHD · UNIVERSITY OF ILLINOIS AT CHICAGO · PI FAZLEABAS, ASGERALLY T. · 2002 to 2011
$13.1M
NICHD NIH HHS HD40093NICHD NIH HHS U54 HD040093
6 · The paper itself

Abstract

objectiveInflammation and proteolysis crucially contribute to myocardial ischemia and reperfusion injury. The extracellular matrix metalloproteinase inducer EMMPRIN (CD147) and its ligand cyclophilin A (CyPA) may be involved in both processes. The aim of the study was to characterize the role of the CD147 and CyPA interplay in myocardial ischemia/reperfusion (I/R) injury. METHODS AND

resultsImmunohistochemistry showed enhanced expression of CD147 and CyPA in myocardial sections from human autopsies of patients who had died from acute myocardial infarction and from mice at 24 hours after I/R. At 24 hours and 7 days after I/R, the infarct size was reduced in CD147(+/-) mice vs CD147(+/+) mice (C57Bl/6), in mice (C57Bl/6) treated with monoclonal antibody anti-CD147 vs control monoclonal antibody, and in CyPA(-/-) mice vs CyPA(+/+) mice (129S6/SvEv), all of which are associated with reduced monocyte and neutrophil recruitment at 24 hours and with a preserved systolic function at 7 days. The combination of CyPA(-/-) mice with anti-CD147 treatment did not yield further protection compared with either inhibition strategy alone. In vitro, treatment with CyPA induced monocyte chemotaxis in a CD147- and phosphatidylinositol 3-kinase-dependent manner and induced monocyte rolling and adhesion to endothelium (human umbilical vein endothelial cells) under flow in a CD147-dependent manner.

conclusionCD147 and its ligand CyPA are inflammatory mediators after myocardial ischemia and reperfusion and represent potential targets to prevent myocardial I/R injury.

Indexed as

SystoleAnimalsBasiginCell AdhesionCell MovementCyclophilin AHumansMacrophagesMiceMice, Inbred C57BLMyocardial InfarctionMyocardial IschemiaMyocardial Reperfusion InjuryNeutrophilsBasiginBSG protein, humanBsg protein, mouseCyclophilin A

Identifiers

PMID21441138
PMCPMC3113549
OpenAlexW2145700523

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.