Evidence map›Paper›PMID 26241027›Full record

ReviewTranslational research : the journal of laboratory and clinical medicine2016

Inflammation as a therapeutic target in myocardial infarction: learning from past failures to meet future challenges.

Amit Saxena, Ilaria Russo, Nikolaos G Frangogiannis

Open access · greenAbstract readReview
In one paragraph

Review in Translational research : the journal of laboratory and clinical medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
10.2field-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

97 citing papers in PubMed, 149 citations in OpenAlex.

  1. Article
  2. Review
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  8. Review
  9. Article
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  12. Cardiac preservation usingFrontiers in cardiovascular medicine · 2025
    Article
  13. Article
  14. Targeting GαBasic research in cardiology · 2024
    Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

37 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

3 authors at 1 institution in 1 country.

Amit SaxenaDepartment of Medicine (Cardiology), The Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, NY.
Ilaria RussoDepartment of Medicine (Cardiology), The Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, NY.
Nikolaos G FrangogiannisDepartment of Medicine (Cardiology), The Wilf Family Cardiovascular Research Institute, Albert Einstein College of Medicine, Bronx, NY. Electronic address: nikolaos.frangogiannis@einstein.yu.edu.
Albert Einstein College of Medicine · US

Funding

Translational Research CoreP30DK020541 · NIDDK · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI STREAMSON C CHUA · 2015 to 2026
$27.7M
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 HL085440NHLBI NIH HHS R01 HL76246NHLBI NIH HHS R01 HL85440NIDDK NIH HHS P30 DK020541
6 · The paper itself

Abstract

In the infarcted myocardium, necrotic cardiomyocytes release danger signals, activating an intense inflammatory response. Inflammatory pathways play a crucial role in regulation of a wide range of cellular processes involved in injury, repair, and remodeling of the infarcted heart. Proinflammatory cytokines, such as tumor necrosis factor α and interleukin 1, are markedly upregulated in the infarcted myocardium and promote adhesive interactions between endothelial cells and leukocytes by stimulating chemokine and adhesion molecule expression. Distinct pairs of chemokines and chemokine receptors are implicated in recruitment of various leukocyte subpopulations in the infarcted myocardium. For more than the past 30 years, extensive experimental work has explored the role of inflammatory signals and the contributions of leukocyte subpopulations in myocardial infarction. Robust evidence derived from experimental models of myocardial infarction has identified inflammatory targets that may attenuate cardiomyocyte injury or protect from adverse remodeling. Unfortunately, attempts to translate the promising experimental findings to clinical therapy have failed. This review article discusses the biology of the inflammatory response after myocardial infarction, attempts to identify the causes for the translational failures of the past, and proposes promising new therapeutic directions. Because of their potential involvement in injurious, reparative, and regenerative responses, inflammatory cells may hold the key for design of new therapies in myocardial infarction.

Indexed as

AnimalsAnti-Inflammatory AgentsCytokinesHumansInflammationMyocardial InfarctionSignal TransductionWound HealingAnti-Inflammatory AgentsCytokines

Identifiers

PMID26241027
PMCPMC4684426
OpenAlexW918747366

What OpenQuestion holds

Textmetadata
LicenceTDM
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.