Evidence map›Paper›PMID 34257332›Full record

ArticleScientific reports2021

Haematopoietic and cardiac GPR55 synchronize post-myocardial infarction remodelling.

Sarah-Lena Puhl, Michael Hilby, Michael Kohlhaas, Linus M Keidel, Yvonne Jansen, Michael Hristov, Jakob Schindler, Christoph Maack, Sabine Steffens

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

13 citing papers in PubMed, 17 citations in OpenAlex.

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  13. Metabolic Consequences of Gestational Cannabinoid Exposure.International journal of molecular sciences · 2021
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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

9 authors at 3 institutions in 1 country.

Sarah-Lena PuhlInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-Universität (LMU) Munich, Pettenkoferstr. 9, 80336, Munich, Germany.
Michael HilbyInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-Universität (LMU) Munich, Pettenkoferstr. 9, 80336, Munich, Germany.
Michael KohlhaasComprehensive Heart Failure Center, University Clinic Würzburg, Würzburg, Germany.
Linus M KeidelInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-Universität (LMU) Munich, Pettenkoferstr. 9, 80336, Munich, Germany.
Yvonne JansenInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-Universität (LMU) Munich, Pettenkoferstr. 9, 80336, Munich, Germany.
Michael HristovInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-Universität (LMU) Munich, Pettenkoferstr. 9, 80336, Munich, Germany.
Jakob SchindlerInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-Universität (LMU) Munich, Pettenkoferstr. 9, 80336, Munich, Germany.
Christoph MaackComprehensive Heart Failure Center, University Clinic Würzburg, Würzburg, Germany.
Sabine SteffensInstitute for Cardiovascular Prevention (IPEK), Ludwig-Maximilians-Universität (LMU) Munich, Pettenkoferstr. 9, 80336, Munich, Germany. Sabine.steffens@med.uni-muenchen.de.
Ludwig-Maximilians-Universität München · DEUniversitätsklinikum Würzburg · DEGerman Centre for Cardiovascular Research · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

While classical cannabinoid receptors are known to crucially impact on myocardial infarction (MI) repair, a function of the cannabinoid-sensitive receptor GPR55 herein is poorly understood. We investigated the role of GPR55 in cardiac physiology and post-MI inflammation and remodelling. Global GPR55-/- and wildtype (WT) mice were basally characterized or assigned to 1, 3 or 28 days permanent MI and subsequently analysed via pro-inflammatory and pro-hypertrophic parameters. GPR55-/- deficiency was basally associated with bradycardia, increased diastolic LV volume and sarcomere length and a subtle inflammatory phenotype. While infarct size and myeloid cell infiltration were unaffected by GPR55 depletion, acute cardiac chemokine production was prolonged post-MI. Concurrently, GPR55-/- hearts exhibited a premature expansion of pro-reparative and phagocytic macrophages paralleled by early up-regulation of extracellular matrix (ECM) factors 3 days post-MI, which could be mimicked by sole haematopoietic GPR55 depletion. Moreover, global GPR55 deficiency mitigated MI-induced foetal gene re-programming and cardiomyocyte hypertrophy, culminating in aggravated LV dilatation and infarct expansion. GPR55 regulates cardiac homeostasis and ischaemia responses by maintaining adequate LV filling and modulating three crucial processes post-MI: wound healing kinetics, cardiomyocyte hypertrophy and maladaptive remodelling.

Indexed as

Myocardial InfarctionReceptors, CannabinoidVentricular RemodelingAnimalsDisease Models, AnimalInflammationMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMyocardiumMyocytes, CardiacGPR55 protein, mouseReceptors, Cannabinoid

Identifiers

PMID34257332
PMCPMC8277802
OpenAlexW3157456475

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.