Evidence map›Paper›PMID 32415537›Full record

ReviewJournal of cardiovascular translational research2021

Chemokines in Myocardial Infarction.

Bijun Chen, Nikolaos G Frangogiannis

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of cardiovascular translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed, 2 pooled it
9.1field-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

63 citing papers in PubMed, 2 syntheses or guidelines pooled it, 96 citations in OpenAlex.

  1. Pooled it
  2. Guidelines for in vivo mouse models of myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2021
    Guideline
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  12. Article
  13. Neutrophil-secreted CHI3L1 exacerbates cardiac dysfunction and inflammation after myocardial infarction.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  14. Review
  15. Article
  16. Article
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  20. Article

3 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 1 country.

Bijun ChenThe Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, 1300 Morris Park Avenue Forchheimer G46B, Bronx, NY, USA.
Nikolaos G FrangogiannisThe Wilf Family Cardiovascular Research Institute, Department of Medicine (Cardiology), Albert Einstein College of Medicine, 1300 Morris Park Avenue Forchheimer G46B, Bronx, NY, USA. nikolaos.frangogiannis@einstein.yu.edu.
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
Regulation of the TGF-beta superfamily in the remodeling and failing heartR01HL149407 · NHLBI · ALBERT EINSTEIN COLLEGE OF MEDICINE · PI FRANGOGIANNIS, NIKOLAOS G · 2020 to 2023
$2.2M
NHLBI NIH HHS R01 HL149407NHLBI NIH HHS R01 HL76246NHLBI NIH HHS R01 HL85440
6 · The paper itself

Abstract

In the infarcted myocardium, cardiomyocyte necrosis triggers an intense inflammatory reaction that not only is critical for cardiac repair, but also contributes to adverse remodeling and to the pathogenesis of heart failure. Both CC and CXC chemokines are markedly induced in the infarcted heart, bind to endothelial glycosaminoglycans, and regulate leukocyte trafficking and function. ELR+ CXC chemokines (such as CXCL8) control neutrophil infiltration, whereas CC chemokines (such as CCL2) mediate recruitment of mononuclear cells. Moreover, some members of the chemokine family (such as CXCL10 and CXCL12) may mediate leukocyte-independent actions, directly modulating fibroblast and vascular cell function. This review manuscript discusses our understanding of the role of the chemokines in regulation of injury, repair, and remodeling following myocardial infarction. Although several chemokines may be promising therapeutic targets in patients with myocardial infarction, clinical implementation of chemokine-based therapeutics is hampered by the broad effects of the chemokines in both injury and repair.

Indexed as

AnimalsBiomarkersChemokinesDisease ProgressionHumansMyocardial InfarctionMyocardiumVentricular RemodelingBiomarkersChemokinesCardiac remodelingCCL2ChemokineCXCL12LeukocyteMyocardial infarction

Identifiers

PMID32415537
OpenAlexW3025787481

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.