Evidence map›Paper›PMID 29394499›Full record

ReviewBritish journal of pharmacology2018

Anti-inflammatory therapies in myocardial infarction: failures, hopes and challenges.

Shuaibo Huang, Nikolaos G Frangogiannis

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
165citing papers in PubMed, 4 pooled it
17.6field-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

165 citing papers in PubMed, 4 syntheses or guidelines pooled it, 275 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Trial
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Identification of anoikis-related biomarkers linking immune infiltration to acute myocardial infarction.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas · 2026
    Article
  20. Frontiers in immunology · 2026
    Review

105 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

2 authors at 1 institution in 2 countries.

Shuaibo HuangThe Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx, NY, 10461, USA.
Nikolaos G FrangogiannisThe Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, Bronx, NY, 10461, USA.ORCID 0000-0002-8186-5131
Albert Einstein College of Medicine · US

Funding

Chemokines in Healing Myocardial InfarctsR01HL076246 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI Nikolaos G Frangogiannis · 2005 to 2026
$9.5M
Resolution of Inflammation in healing Myocardial InfarctsR01HL085440 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI FRANGOGIANNIS, NIKOLAOS G · 2008 to 2025
$8.5M
NHLBI NIH HHS R01 HL076246NHLBI NIH HHS R01 HL085440
6 · The paper itself

Abstract

In the infarcted heart, the damage-associated molecular pattern proteins released by necrotic cells trigger both myocardial and systemic inflammatory responses. Induction of chemokines and cytokines and up-regulation of endothelial adhesion molecules mediate leukocyte recruitment in the infarcted myocardium. Inflammatory cells clear the infarct of dead cells and matrix debris and activate repair by myofibroblasts and vascular cells, but may also contribute to adverse fibrotic remodelling of viable segments, accentuate cardiomyocyte apoptosis and exert arrhythmogenic actions. Excessive, prolonged and dysregulated inflammation has been implicated in the pathogenesis of complications and may be involved in the development of heart failure following infarction. Studies in animal models of myocardial infarction (MI) have suggested the effectiveness of pharmacological interventions targeting the inflammatory response. This article provides a brief overview of the cell biology of the post-infarction inflammatory response and discusses the use of pharmacological interventions targeting inflammation following infarction. Therapy with broad anti-inflammatory and immunomodulatory agents may also inhibit important repair pathways, thus exerting detrimental actions in patients with MI. Extensive experimental evidence suggests that targeting specific inflammatory signals, such as the complement cascade, chemokines, cytokines, proteases, selectins and leukocyte integrins, may hold promise. However, clinical translation has proved challenging. Targeting IL-1 may benefit patients with exaggerated post-MI inflammatory responses following infarction, not only by attenuating adverse remodelling but also by stabilizing the atherosclerotic plaque and by inhibiting arrhythmia generation. Identification of the therapeutic window for specific interventions and pathophysiological stratification of MI patients using inflammatory biomarkers and imaging strategies are critical for optimal therapeutic design.

Indexed as

AnimalsAnti-Inflammatory AgentsHumansImmunologic FactorsInflammationInflammation MediatorsMolecular Targeted TherapyMyocardial InfarctionAnti-Inflammatory AgentsImmunologic FactorsInflammation Mediators

Identifiers

PMID29394499
PMCPMC5901181
OpenAlexW2790209689

What OpenQuestion holds

Textmetadata
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.