ReviewInflammation research : official journal of the European Histamine Research Society ... [et al.]2025
The dual role of ATF3 in myocardial repair through macrophage regulation.
Review in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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Who cites it
2 citing papers in PubMed.
- The Murine Antimicrobial Peptide CRAMP Alleviates Neuroinflammation By Downregulating the cGAS-STING Signalling Pathway.Molecular neurobiology · 2026Article
- Identification of ATF3 as a Potential Key Biomarker for Hypertensive Nephropathy via Single-Cell Transcriptome Sequencing.Inflammation · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
objectiveIschemic heart disease (IHD) is one of the leading causes of death globally, and the process of myocardial repair after myocardial infarction (MI) is complex and crucial. Recent studies have underscored the pivotal role of cardiac-resident macrophages in the salvage of infarcted myocardium. This literature review summarizes recent findings on the central regulatory function of the activating transcription factor 3 (ATF3) in regulating macrophage behavior and macrophage-cardiomyocyte crosstalk during post-MI myocardial repair.
methodsA comprehensive review of recent experimental and translational studies was conducted, focusing on ATF3 mediated regulation of macrophage activation, polarization, functional plasticity, and intercellular communication in the context of ischemic heart injury and repair.
resultsATF3, a stress-responsive transcription factor, is a key mediator in oxidative stress and ischemic injury responses across diverse cellular milieus.The complexity of ATF3's role in regulating macrophage involvement in myocardial repair stems from multiple factors: the cell types expressing ATF3 can affect its function; the stage of disease progression may alter ATF3's role; and ATF3's activity is regulated not only at the expression level but also by post-translational modifications such as ubiquitination and SUMOylation. These factors collectively contribute to the intricate regulation of ATF3. Moreover, the origin of macrophages also dictates their multidimensional role in myocardial repair.
conclusionsThe ATF3-macrophage axis represents a critical regulatory network in post-MI myocardial repair. Elucidating its context dependent and cell specific mechanisms may provide novel therapeutic insights for modulating post infarction inflammation and improving cardiac repair outcomes.
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Registered trials
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