Evidence map›Paper›PMID 29167227›Full record

ArticleCirculation2018

Pericardial Adipose Tissue Regulates Granulopoiesis, Fibrosis, and Cardiac Function After Myocardial Infarction.

Michael Horckmans, Mariaelvy Bianchini, Donato Santovito, Remco T A Megens, Jean-Yves Springael, Irene Negri, Michele Vacca, Marco Di Eusanio, Antonio Moschetta, Christian Weber and 2 more

Registry-linked trialOpen access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Circulation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06557811 (Effect of Oral Semaglutide on Epicardial and Pericoronary Adipose Tissues in Type 2 Diabetes After Myocardial Infarction), which is not on this map. Cited by 112 papers.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed
8.6field-weighted citation impact, top 2% 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.

NCT06557811 phase4not yet recruitingstarted 2024, after this paper: background citation

Effect of Oral Semaglutide on Epicardial and Pericoronary Adipose Tissues in Type 2 Diabetes After Myocardial Infarction: a Randomized and Double-blind Clinical Trial

Ran2024Enrolled88Registered outcomes26Posted comparisons0ConditionsAcute Myocardial Infarction, Diabetic PatientsArmssemaglutide
PMID 28814394PMID 33778665PMID 30287946PMID 29704210PMID 29675684PMID 29098638PMID 28762019PMID 28721155PMID 28701474PMID 28444175PMID 28253918PMID 28246237other papers from this trial
Open the trial in the graph
3 · Its place in the literature

Who cites it

112 citing papers in PubMed, 167 citations in OpenAlex.

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52 more citing papers are in PubMed but not listed here.

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

12 authors at 3 institutions in 3 countries.

Michael HorckmansBrussels, Belgium (M.H., J.-Y.S., I.N.).
Mariaelvy BianchiniInstitute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany (M.B., D.S., R.T.A.M., C.W., J.D., S.S.).
Donato SantovitoInstitute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany (M.B., D.S., R.T.A.M., C.W., J.D., S.S.).
Remco T A MegensInstitute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany (M.B., D.S., R.T.A.M., C.W., J.D., S.S.).
Jean-Yves SpringaelBrussels, Belgium (M.H., J.-Y.S., I.N.).
Irene NegriBrussels, Belgium (M.H., J.-Y.S., I.N.).
Michele VaccaCardiovascular Research Institute Maastricht, Maastricht University, Netherlands. Department of Interdisciplinary Medicine (M.V.).
Marco Di EusanioCardiovascular Department, "S.Orsola Malpighi" Hospital, University of Bologna, Italy (M.D.E.).
Antonio MoschettaClinica Medica "C. Frugoni," (A.M.).
Christian WeberInstitute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany (M.B., D.S., R.T.A.M., C.W., J.D., S.S.).
Johan DucheneInstitute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany (M.B., D.S., R.T.A.M., C.W., J.D., S.S.).
Sabine SteffensInstitute for Cardiovascular Prevention, Ludwig-Maximilians-University, Munich, Germany (M.B., D.S., R.T.A.M., C.W., J.D., S.S.). sabine.steffens@med.uni-muenchen.de.
Clínica Santa María · COLudwig-Maximilians-Universität München · DEMaastricht University · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe pericardial adipose tissue (AT) contains a high density of lymphoid clusters. It is unknown whether these clusters play a role in post-myocardial infarction (MI) inflammatory responses and cardiac outcome.

methodsLymphoid clusters were examined in epicardial AT of humans with or without coronary artery disease. Murine pericardial lymphoid clusters were visualized in mice subjected to coronary artery ligation. To study the relevance of pericardial clusters during inflammatory responses after MI, we surgically removed the pericardial AT and performed B-cell depletion and granulocyte-macrophage colony-stimulating factor blockade. Leukocytes in murine hearts, pericardial AT, spleen, mediastinal lymph nodes, and bone marrow were quantified by flow cytometry. Cannabinoid receptor CB2 (CB2

resultsWe identified larger B-cell clusters in epicardial AT of human patients with coronary artery disease in comparison with controls without coronary artery disease. Infarcted mice also had larger pericardial clusters and 3-fold upregulated numbers of granulocyte-macrophage colony-stimulating factor-producing B cells within pericardial AT, but not spleen or lymph nodes. This was associated with higher DC and T-cell counts in pericardial AT, which outnumbered DCs and T cells in lymph nodes. Analysis of DC maturation markers, tracking experiments with fluorescently labeled cells, and use of CCR7-deficient mice suggested that activated DCs migrate from infarcts into pericardial AT via CCR7. B-cell depletion or granulocyte-macrophage colony-stimulating factor neutralization inhibited DC and T-cell expansion within pericardial AT, and translated into reduced bone marrow granulopoiesis and cardiac neutrophil infiltration 3 days after MI. The relevance of the pericardial AT in mediating all these effects was confirmed by removal of pericardial AT and ex vivo coculture with pericardial AT and granulocyte progenitors. Finally, enhanced fibrosis and worsened ejection fraction in CB2

conclusionsOur findings unveil a new mechanism by which the pericardial AT coordinates immune cell activation, granulopoiesis, and outcome after MI.

Indexed as

Adipose TissueAnimalsCell DifferentiationDisease Models, AnimalFemaleFibrosisGranulocytesHumansImmunity, InnateMiceMice, Inbred C57BLMice, KnockoutMyocardial InfarctionMyocardiumPericardiumReceptor, Cannabinoid, CB2Ccr7 protein, mouseReceptor, Cannabinoid, CB2Receptors, CCR7B-lymphocytesdendritic cellsgranulocyte-macrophage colony-stimulating factorhematopoietic stem cellslymphoid tissuestem cells

Identifiers

PMID29167227
OpenAlexW2770357646

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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 Socratic graph.