Evidence map›Paper›PMID 31841135›Full record

ReviewCardiovascular research2020

Cardiac monocytes and macrophages after myocardial infarction.

Claire Peet, Aleksandar Ivetic, Daniel I Bromage, Ajay M Shah

Open access · hybridAbstract readReview
In one paragraph

Review in Cardiovascular research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 355 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
355citing papers in PubMed, 2 pooled it
31.1field-weighted citation impact, top 1% 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

355 citing papers in PubMed, 2 syntheses or guidelines pooled it, 571 citations in OpenAlex.

  1. Pooled it
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  13. Immunometabolic Remodeling in Ischemic and Non-Ischemic Heart Failure.Journal of cardiovascular translational research · 2026
    Review
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295 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

4 authors at 1 institution in 1 country.

Claire PeetSchool of Cardiovascular Medicine and Sciences, James Black Centre, King's College London BHF Centre of Excellence, 125 Coldharbour Lane, London SE5 9NU, UK.
Aleksandar IveticSchool of Cardiovascular Medicine and Sciences, James Black Centre, King's College London BHF Centre of Excellence, 125 Coldharbour Lane, London SE5 9NU, UK.
Daniel I BromageSchool of Cardiovascular Medicine and Sciences, James Black Centre, King's College London BHF Centre of Excellence, 125 Coldharbour Lane, London SE5 9NU, UK.
Ajay M ShahSchool of Cardiovascular Medicine and Sciences, James Black Centre, King's College London BHF Centre of Excellence, 125 Coldharbour Lane, London SE5 9NU, UK.
King's College London · GB

Funding

British Heart Foundation CH/1999001/11735British Heart Foundation RE/18/2/34213British Heart Foundation RG/13/11/30384
6 · The paper itself

Abstract

Improvements in early interventions after acute myocardial infarction (AMI), notably, the increased use of timely reperfusion therapy, have increased survival dramatically in recent decades. Despite this, maladaptive ventricular remodelling and subsequent heart failure (HF) following AMI remain a significant clinical challenge, particularly because several pre-clinical strategies to attenuate remodelling have failed to translate into clinical practice. Monocytes and macrophages, pleiotropic cells of the innate immune system, are integral in both the initial inflammatory response to injury and subsequent wound healing in many tissues, including the heart. However, maladaptive immune cell behaviour contributes to ventricular remodelling in mouse models, prompting experimental efforts to modulate the immune response to prevent the development of HF. Seminal work in macrophage biology defined macrophages as monocyte-derived cells that are comprised of two populations, pro-inflammatory M1 macrophages and reparative M2 macrophages, and initial investigations into cardiac macrophage populations following AMI suggested they aligned well to this model. However, more recent data, in the heart and other tissues, demonstrate remarkable heterogeneity and plasticity in macrophage development, phenotype, and function. These recent insights into macrophage biology may explain the failure of non-specific immunosuppressive strategies and offer novel opportunities for therapeutic targeting to prevent HF following AMI. Here, we summarize the traditional monocyte-macrophage paradigm, experimental evidence for the significance of these cells in HF after AMI, and the potential relevance of emerging evidence that refutes canonical models of monocyte and macrophage biology.

Indexed as

Ventricular RemodelingAnimalsHumansMacrophagesMonocytesMyocardial InfarctionMyocardiumPhenotypeMacrophageMonocyteMyocardial infarction

Identifiers

PMID31841135
PMCPMC7177720
OpenAlexW2995705978

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.