Evidence map›Paper›PMID 30543467›Full record

ArticleHypertension (Dallas, Tex. : 1979)2019

Macrophage Mineralocorticoid Receptor Is a Pleiotropic Modulator of Myocardial Infarct Healing.

Daniela Fraccarollo, Svenja Thomas, Claus-Jürgen Scholz, Denise Hilfiker-Kleiner, Paolo Galuppo, Johann Bauersachs

Open access · hybridAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

26 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
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  5. Prostaglandin DCells · 2025
    Article
  6. Review
  7. Vitamin A deficiency attenuates cardiac rupture inFrontiers in cardiovascular medicine · 2025
    Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
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  17. The role of endogenous Smad7 in regulating macrophage phenotype following myocardial infarction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  18. Review
  19. Article
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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

6 authors at 1 institution in 1 country.

Daniela FraccarolloFrom the Department of Cardiology and Angiology, Hannover Medical School, Germany (D.F., S.T., D.H.-K., P.G., J.B.).
Svenja ThomasFrom the Department of Cardiology and Angiology, Hannover Medical School, Germany (D.F., S.T., D.H.-K., P.G., J.B.).
Claus-Jürgen ScholzCore Unit SysMed, University of Würzburg, Germany (C.-J.S.).
Denise Hilfiker-KleinerFrom the Department of Cardiology and Angiology, Hannover Medical School, Germany (D.F., S.T., D.H.-K., P.G., J.B.).
Paolo GaluppoFrom the Department of Cardiology and Angiology, Hannover Medical School, Germany (D.F., S.T., D.H.-K., P.G., J.B.).
Johann BauersachsFrom the Department of Cardiology and Angiology, Hannover Medical School, Germany (D.F., S.T., D.H.-K., P.G., J.B.).
Medizinische Hochschule Hannover · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myocardial infarction (MI) is a major cause of death worldwide. Here, we identify the macrophage MR (mineralocorticoid receptor) as a crucial pathogenic player in cardiac wound repair after MI. Seven days after left coronary artery ligation, mice with myeloid cell-restricted MR deficiency compared with WT (wild type) controls displayed improved cardiac function and remodeling associated with enhanced infarct neovascularization and scar maturation. Gene expression profiling of heart-resident and infarct macrophages revealed that MR deletion drives macrophage differentiation in the ischemic microenvironment toward a phenotype outside the M1/M2 paradigm, with regulation of multiple interrelated factors controlling wound healing and tissue repair. Mechanistic and functional data suggest that inactivation of the macrophage MR promotes myocardial infarct healing through enhanced efferocytosis of neutrophils, the suppression of free radical formation, and the modulation of fibroblast activation state. Crucially, targeted delivery of MR antagonists to macrophages, with a single administration of RU28318 or eplerenone-containing liposomes at the onset of MI, improved the healing response and protected against cardiac remodeling and functional deterioration, offering an effective and unique therapeutic strategy for cardiac repair.

Indexed as

Myocardial InfarctionMyocardiumReceptors, MineralocorticoidWound HealingAnimalsCell DifferentiationCellular MicroenvironmentDisease Models, AnimalEplerenoneGene Expression ProfilingHeartLiposomesMacrophagesMiceMineralocorticoid Receptor AntagonistsVentricular RemodelingEplerenoneLiposomesMineralocorticoid Receptor AntagonistsReceptors, Mineralocorticoidliposomesmacrophagesmyocardial infarctionreceptors, mineralocorticoidwound healing

Identifiers

PMID30543467
PMCPMC6291261
OpenAlexW2901396500

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.