ReviewFrontiers in cardiovascular medicine2019
The Role of Macrophages in the Infarcted Myocardium: Orchestrators of ECM Remodeling.
Review in Frontiers in cardiovascular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 1 of them a synthesis that pooled 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.
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.
Who cites it
66 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.
- Trace Elements and Depressive Symptoms in Coronary Artery Disease: A Systematic Review of Sparse and Predominantly Indirect Evidence.International journal of molecular sciences · 2026Pooled it
- Full-field analysis indicates late reperfusion therapy broadens and mechanically smooths the borderzone during post-infarction inflammation.Acta biomaterialia · 2026Article
- Macrophage-Dependent Intercellular Crosstalk in Multiphenotypic Heart Failure With Preserved Ejection Fraction.Journal of the American Heart Association · 2026Review
- Microfluidic Modeling of Macrophage-Induced Cardiac Inflammation Using NF-κB Reporter Cardiomyocytes.Advanced healthcare materials · 2026Article
- New Insights into the Anti-Aging Mechanism of Collagen Peptides-Emphasis on Lysosomes and Mitochondria Function.Molecules (Basel, Switzerland) · 2026Review
- Mitochondrial Targeting by Elamipretide Improves Myocardial Bioenergetics Without Translating into Functional Benefits in HFpEF.International journal of molecular sciences · 2026Article
- Loss of fibronectin fiber tension is inherent to ECM remodeling in human myocarditis and post-inflammatory fibrosis.Matrix biology plus · 2025Article
- Circular RNA Cdr1as Modulates Macrophage-Mediated Cardiac Reparative Function.Circulation research · 2025Article
- Dynamics of Macrophage Polarization Reveal Unique Phenotypes During Mouse Postpartum Uterine Remodeling.bioRxiv : the preprint server for biology · 2025Article
- Review
- Modulation of Macrophage Polarization by Traditional Chinese Medicine in HFpEF: A Review of Mechanisms and Therapeutic Potentials.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Integrated MicroRNA-mRNA Sequencing Analysis Identifies Regulators and Networks Involved in Feline Hypertrophic Cardiomyopathy.International journal of molecular sciences · 2025Article
- The Role of C-Reactive Protein in Acute Myocardial Infarction: Unmasking Diagnostic, Prognostic, and Therapeutic Insights.Journal of clinical medicine · 2025Review
- Tissue Repair Mechanisms of Dental Pulp Stem Cells: A Comprehensive Review from Cutaneous Regeneration to Mucosal Healing.Current issues in molecular biology · 2025Review
- Innovative approaches to boost mesenchymal stem cells efficacy in myocardial infarction therapy.Materials today. Bio · 2025Review
- From innovation to clinic: Emerging strategies harnessing electrically conductive polymers to enhance electrically stimulated peripheral nerve repair.Materials today. Bio · 2025Article
- Matrisome remodeling in the myocardium of hypertrophic cardiomyopathy; novel targets for molecular diagnostics.Frontiers in cell and developmental biology · 2025Review
- Macrophage Membrane-Coated Nanocarriers in Myocardial Infarction: A Paradigm Shift in Targeted Cardiac Therapy.International journal of nanomedicine · 2025Review
- Loss of PKM2 dysregulates inflammatory signaling in the infarcted murine heart.Physiological reports · 2025Article
- Engineered macrophages: an "Intelligent Repair" cellular machine for heart injury.Cell regeneration (London, England) · 2024Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial infarction is the most common form of acute cardiac injury attributing to heart failure. While there have been significant advances in current therapies, mortality and morbidity remain high. Emphasis on inflammation and extracellular matrix remodeling as key pathological factors has brought to light new potential therapeutic targets including macrophages which are central players in the inflammatory response following myocardial infarction. Blood derived and tissue resident macrophages exhibit both a pro- and anti-inflammatory phenotype, essential for removing injured tissue and facilitating repair, respectively. Sustained activation of pro-inflammatory macrophages evokes extensive remodeling of cardiac tissue through secretion of matrix proteases and activation of myofibroblasts. As the heart continues to employ methods of remodeling and repair, a destructive cycle prevails ultimately leading to deterioration of cardiac function and heart failure. This review summarizes not only the traditionally accepted role of macrophages in the heart but also recent advances that have deepened our understanding and appreciation of this dynamic cell. We discuss the role of macrophages in normal and maladaptive matrix remodeling, as well as studies to date which have aimed to target the inflammatory response in combatting excessive matrix deposition and subsequent heart failure.
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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.