ArticleJournal of cellular and molecular medicine2009
Classically and alternatively activated macrophages contribute to tissue remodelling after myocardial infarction.
Article in Journal of cellular and molecular medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers.
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Who cites it
128 citing papers in PubMed, 277 citations in OpenAlex.
- Trial
- Increased NETosis in Patients With Heart Failure Is Associated With Macrophage Activation Towards a Proinflammatory Phenotype.Journal of cellular and molecular medicine · 2026Article
- Full-field analysis indicates late reperfusion therapy broadens and mechanically smooths the borderzone during post-infarction inflammation.Acta biomaterialia · 2026Article
- Macrophage PRMT9 Ameliorates Acute Myocardial Infarction by Promoting Symmetric Dimethylation and Degradation of STAT1.Circulation · 2026Article
- Distinct immunometabolic signatures of type 1 versus type 2 diabetes in a murine model of myocardial infarction.Cardiovascular diabetology · 2026Article
- Contribution of monocyte subpopulations to the pathogenesis and therapy outcome of type 1 diabetes management in pediatric patients.Frontiers in immunology · 2026Article
- Sophoricoside enhances reparative macrophage polarization to promote cardiac repair postmyocardial infarction through PPAR-γ.Coronary artery disease · 2026Article
- Dietary Nitrate Prevents Cardiac Dysfunction in HFrEF by Improving Hemodynamics, Ameliorating Remodeling, and Resolving Inflammation.Acta physiologica (Oxford, England) · 2025Article
- Pannexin1 via P2rx7/amphiregulin contributes to cardiac fibrosis post myocardial infarction.Journal of molecular histology · 2025Article
- Antagonizing CCR2 With Propagermanium Leads to Altered Distribution of Macrophage Subsets and Favorable Tissue Remodeling After Myocardial Infarction in Mice.Cardiovascular therapeutics · 2025Article
- Unraveling Macrophage Polarization: Functions, Mechanisms, and "Double-Edged Sword" Roles in Host Antiviral Immune Responses.International journal of molecular sciences · 2024Review
- Cardioimmunology in Health and Diseases: Impairment of the Cardio-Spleno-Bone Marrow Axis Following Myocardial Infarction in Diabetes Mellitus.International journal of molecular sciences · 2024Article
- Serotonin-2 Receptor Agonists Produce Anti-inflammatory Effects through Functionally Selective Mechanisms That Involve the Suppression of Disease-Induced Arginase 1 Expression.ACS pharmacology & translational science · 2024Article
- Impact of age and sex on myelopoiesis and inflammation during myocardial infarction.Journal of molecular and cellular cardiology · 2024Review
- Decades Long Involvement of THP-1 Cells as a Model for Macrophage Research: A Comprehensive Review.Anti-inflammatory & anti-allergy agents in medicinal chemistry · 2024Review
- Single-cell RNA sequencing reveals S100a9Theranostics · 2024Article
- Target and Cell Therapy for Atherosclerosis and CVD.International journal of molecular sciences · 2023Review
- Hydrogen Attenuates Inflammation by Inducing Early M2 Macrophage Polarization in Skin Wound Healing.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Review on Additives in Hydrogels for 3D Bioprinting of Regenerative Medicine: From Mechanism to Methodology.Pharmaceutics · 2023Review
- Don't go breakin' my heart: cardioprotective alterations to the mechanical and structural properties of reperfused myocardium during post-infarction inflammation.Biophysical reviews · 2023Review
68 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An important goal in cardiology is to minimize myocardial necrosis and to support a discrete but resilient scar formation after myocardial infarction (MI). Macrophages are a type of cells that influence cardiac remodelling during MI. Therefore, the goal of the present study was to investigate their transcriptional profile and to identify the type of activation during scar tissue formation. Ligature of the left anterior descending coronary artery was performed in mice. Macrophages were isolated from infarcted tissue using magnetic cell sorting after 5 days. The total RNA of macrophages was subjected to microarray analysis and compared with RNA from MI and LV-control. mRNA abundance of relevant targets was validated by quantitative real-time PCR 2, 5 and 10 days after MI (qRT-PCR). Immunohistochemistry was performed to localize activation type-specific proteins. The genome scan revealed 68 targets predominantly expressed by macrophages after MI. Among these targets, an increased mRNA abundance of genes, involved in both the classically (tumour necrosis factor alpha, interleukin 6, interleukin 1beta) and the alternatively (arginase 1 and 2, mannose receptor C type 1, chitinase 3-like 3) activated phenotype of macrophages, was found 5 days after MI. This observation was confirmed by qRT-PCR. Using immunohistochemistry, we confirmed that tumour necrosis factor alpha, representing the classical activation, is strongly transcribed early after ligature (2 days). It was decreased after 5 and 10 days. Five days after MI, we found a fundamental change towards alternative activation of macrophages with up-regulation of arginase 1. Our results demonstrate that macrophages are differentially activated during different phases of scar tissue formation after MI. During the early inflammatory phase, macrophages are predominantly classically activated, whereas their phenotype changes during the important transition from inflammation to scar tissue formation into an alternatively activated type.
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Registered trials
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.