Evidence map›Paper›PMID 32489148›Full record

ArticleCirculation2020

Loss of Protease-Activated Receptor 4 Prevents Inflammation Resolution and Predisposes the Heart to Cardiac Rupture After Myocardial Infarction.

Mikhail A Kolpakov, Xinji Guo, Khadija Rafiq, Liudmila Vlasenko, Bahman Hooshdaran, Rachid Seqqat, Tao Wang, Xiaoxuan Fan, Douglas G Tilley, John C Kostyak and 3 more

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
  2. Article
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  4. Article
  5. Korean circulation journal · 2025
    Article
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  15. Platelets in COVID-19 disease: friend, foe, or both?Pharmacological reports : PR · 2022
    Review
  16. Article
  17. Review
  18. 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

13 authors at 4 institutions in 3 countries.

Mikhail A KolpakovCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
Xinji GuoCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
Khadija RafiqThomas Jefferson University, Philadelphia, PA (K.R.).
Liudmila VlasenkoCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
Bahman HooshdaranCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
Rachid SeqqatCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
Tao WangCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
Xiaoxuan FanCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
Douglas G TilleyCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
John C KostyakCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
Satya P KunapuliCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
Steven R HouserCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
Abdelkarim SabriCardiovascular Research Center and Department of Physiology, Temple University School of Medicine, Philadelphia, PA (M.A.K., X.G., L.V., B.H., R.S., T.W., X.F., D.G.T., J.C.K., S.P.K., S.R.H., A.S.).
Temple University · USNorwegian Womens Public Health Association · NOThomas Jefferson University · USX-Fab (Germany) · DE

Funding

Targeting Cbl for Cardiac Repair Post-Myocardial InfarctionR01HL145177 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI SABRI, ABDELKARIM · 2019 to 2022
$2.0M
Protein activated Receptor-4 in Cardiac Rupture after Myocardial InfarctionR01HL139889 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI SABRI, ABDELKARIM · 2018 to 2021
$1.9M
Inflammatory serine proteases and cardiac repair post myocardial infarctionR01HL128446 · NHLBI · TEMPLE UNIV OF THE COMMONWEALTH · PI SABRI, ABDELKARIM · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL128446NHLBI NIH HHS R01 HL139889NHLBI NIH HHS R01 HL145177
6 · The paper itself

Abstract

backgroundCardiac rupture is a major lethal complication of acute myocardial infarction (MI). Despite significant advances in reperfusion strategies, mortality from cardiac rupture remains high. Studies suggest that cardiac rupture can be accelerated by thrombolytic therapy, but the relevance of this risk factor remains controversial.

methodsWe analyzed protease-activated receptor 4 (Par4) expression in mouse hearts with MI and investigated the effects of Par4 deletion on cardiac remodeling and function after MI by echocardiography, quantitative immunohistochemistry, and flow cytometry.

resultsPar4 mRNA and protein levels were increased in mouse hearts after MI and in isolated cardiomyocytes in response to hypertrophic and inflammatory stimuli. Par4-deficient mice showed less myocyte apoptosis, reduced infarct size, and improved functional recovery after acute MI relative to wild-type (WT). Conversely, Par4

conclusionsThese findings reveal essential roles of Par4 in neutrophil apoptosis and inflammation resolution during myocardial healing and point to Par4 inhibition as a potential therapy that should be limited to the acute phases of ischemic insult and avoided for long-term treatment after MI.

Indexed as

Gene Expression RegulationHeart RuptureMyocardial InfarctionAnimalsFemaleInflammationMaleMiceMice, KnockoutMyocardiumReceptors, Thrombinprotease-activated receptor 4Receptors, Thrombinheart ruptureinflammationmyocardial infarctionneutrophilsprotease-activated receptor 4

Identifiers

PMID32489148
PMCPMC9341277
OpenAlexW3029420010

What OpenQuestion holds

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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.