Evidence map›Paper›PMID 30001416›Full record

ArticlePloS one2018

Azithromycin therapy reduces cardiac inflammation and mitigates adverse cardiac remodeling after myocardial infarction: Potential therapeutic targets in ischemic heart disease.

Ahmed Al-Darraji, Dalia Haydar, Lakshman Chelvarajan, Himi Tripathi, Bryana Levitan, Erhe Gao, Vincent J Venditto, John C Gensel, David J Feola, Ahmed Abdel-Latif

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
5.3field-weighted citation impact, top 3% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.

  1. Pooled it
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  5. Progress in macrophage immune regulation of atherosclerosis.American journal of translational research · 2025
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  18. Monocyte recruitment and fate specification after myocardial infarction.American journal of physiology. Cell physiology · 2020
    Review
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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

10 authors at 2 institutions in 1 country.

Ahmed Al-DarrajiGill Heart Institute and Division of Cardiovascular Medicine, University of Kentucky, Lexington, KY, United States of America.
Dalia HaydarCollege of Pharmacy, University of Kentucky, Lexington, KY, United States of America.ORCID 0000-0002-7959-2699
Lakshman ChelvarajanGill Heart Institute and Division of Cardiovascular Medicine, University of Kentucky, Lexington, KY, United States of America.
Himi TripathiGill Heart Institute and Division of Cardiovascular Medicine, University of Kentucky, Lexington, KY, United States of America.
Bryana LevitanGill Heart Institute and Division of Cardiovascular Medicine, University of Kentucky, Lexington, KY, United States of America.
Erhe GaoThe Center for Translational Medicine, Temple University School of Medicine, Philadelphia, PA, United States of America.
Vincent J VendittoCollege of Pharmacy, University of Kentucky, Lexington, KY, United States of America.
John C GenselSpinal Cord and Brain Injury Research Center, Department of Physiology, College of Medicine University of Kentucky, Lexington, KY, United States of America.ORCID 0000-0001-8980-108X
David J FeolaCollege of Pharmacy, University of Kentucky, Lexington, KY, United States of America.
Ahmed Abdel-LatifGill Heart Institute and Division of Cardiovascular Medicine, University of Kentucky, Lexington, KY, United States of America.ORCID 0000-0002-8178-7102
University of Kentucky · USTemple University · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI Bernard Mark Evers · 2013 to 2026
$38.3M
The role of IKKß in linking obesity to adipose tissue inflammation and adipogeneP20GM103527 · NIGMS · UNIVERSITY OF KENTUCKY · PI MORRIS, ANDREW J · 2012 to 2017
$13.7M
Molecular and biochemical basis of LymphangioleiomyomatosisR01HL121266 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI BLENIS, JOHN · 2014 to 2017
$2.0M
Lysophosphatidic Acid Mediates Cardiac Inflammation After Acute InfarctionR01HL138488 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ABDEL-LATIF, AHMED · 2017 to 2021
$1.9M
Alternative macrophage activation in acute Pseudomonas pneumoniaR01AI095307 · NIAID · UNIVERSITY OF KENTUCKY · PI FEOLA, DAVID · 2012 to 2016
$1.8M
Role of Bioactive Lipids in Stem Cell Mobilization and Homing in Cardiac IschemiaR56HL124266 · NHLBI · UNIVERSITY OF KENTUCKY · PI ABDEL-LATIF, AHMED · 2014 to 2014
$375k
NCI NIH HHS P30 CA177558NHLBI NIH HHS R01 HL121266NHLBI NIH HHS R01 HL138488NHLBI NIH HHS R56 HL124266NIAID NIH HHS R01 AI095307NIGMS NIH HHS P20 GM103527
6 · The paper itself

Abstract

introductionAcute myocardial infarction (MI) is a primary cause of worldwide morbidity and mortality. Macrophages are fundamental components of post-MI inflammation. Pro-inflammatory macrophages can lead to adverse cardiac remodeling and heart failure while anti-inflammatory/reparative macrophages enhance tissue healing. Shifting the balance between pro-inflammatory and reparative macrophages post-MI is a novel therapeutic strategy. Azithromycin (AZM), a commonly used macrolide antibiotic, polarizes macrophages towards the anti-inflammatory phenotype, as shown in animal and human studies. We hypothesized that AZM modulates post-MI inflammation and improves cardiac recovery. METHODS AND

resultsMale WT mice (C57BL/6, 6-8 weeks old) were treated with either oral AZM (160 mg/kg/day) or vehicle (control) starting 3 days prior to MI and continued to day 7 post-MI. We observed a significant reduction in mortality with AZM therapy. AZM-treated mice showed a significant decrease in pro-inflammatory (CD45+/Ly6G-/F4-80+/CD86+) and increase in anti-inflammatory (CD45+/Ly6G-/F4-80+/CD206+) macrophages, decreasing the pro-inflammatory/anti-inflammatory macrophage ratio in the heart and peripheral blood as assessed by flow cytometry and immunohistochemistry. Macrophage changes were associated with a significant decline in pro- and increase in anti-inflammatory cytokines. Mechanistic studies confirmed the ability of AZM to shift macrophage response towards an anti-inflammatory state under hypoxia/reperfusion stress. Additionally, AZM treatment was associated with a distinct decrease in neutrophil count due to apoptosis, a known signal for shifting macrophages towards the anti-inflammatory phenotype. Finally, AZM treatment improved cardiac recovery, scar size, and angiogenesis.

conclusionAzithromycin plays a cardioprotective role in the early phase post-MI through attenuating inflammation and enhancing cardiac recovery. Post-MI treatment and human translational studies are warranted to examine the therapeutic applications of AZM.

Indexed as

Administration, OralAnimalsAntigens, DifferentiationAzithromycinCardiotonic AgentsCytokinesInflammationMacrophagesMaleMiceMyocardial InfarctionNeovascularization, PhysiologicAntigens, DifferentiationAzithromycinCardiotonic AgentsCytokines

Identifiers

PMID30001416
PMCPMC6042749
OpenAlexW2871210587

What OpenQuestion holds

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LicenceCC BY
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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.