ReviewAmerican journal of physiology. Cell physiology2022
Macrophages in myocardial infarction.
Review in American journal of physiology. Cell physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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.
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
70 citing papers in PubMed, 90 citations in OpenAlex.
- Targeting the ENO1 metabolic checkpoint via microenvironment-responsive nanotherapeutics promotes postinfarction cardiac repair.Science advances · 2026Article
- Short-chain fatty acids promote post-myocardial infarction cardiac repair via FFAR2-dependent suppression of osteoclast-like macrophage differentiation.Basic research in cardiology · 2026Article
- Increased NETosis in Patients With Heart Failure Is Associated With Macrophage Activation Towards a Proinflammatory Phenotype.Journal of cellular and molecular medicine · 2026Article
- Fate-mapping infiltrating monocytes following experimental myocardial infarction reveals differentiation trajectories in the infarcted heart.The Journal of clinical investigation · 2026Article
- Resibufogenin promotes angiogenesis via the VAV3-mediated ITGA5-VEGF signaling axis in macrophages to alleviate myocardial infarction.Acta pharmacologica Sinica · 2026Article
- From Ischemic Injury to Arrhythmogenic Substrate: Molecular and Histopathological Insights into Post-Infarction Sudden Cardiac Death.Life (Basel, Switzerland) · 2026Review
- Full-field analysis indicates late reperfusion therapy broadens and mechanically smooths the borderzone during post-infarction inflammation.Acta biomaterialia · 2026Article
- MiR-378a-3p Promotes Macrophage Polarization from M1 to M2 for Cardiac Repair after Infarction Via Trem1.Journal of cardiovascular translational research · 2026Article
- Metabolic regulation of macrophage polarization in myocardial infarction: from mechanisms to targeted therapies.Journal of translational medicine · 2026Review
- Macrophages and the Survival of Cardiomyocytes After Myocardial Infarction.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Immunometabolic Remodeling in Ischemic and Non-Ischemic Heart Failure.Journal of cardiovascular translational research · 2026Review
- Molecular Imaging of Macrophages in Cardiovascular Diseases.Molecular imaging and biology · 2026Review
- Flavin adenine dinucleotide increases antioxidant availability and protects neonatal C57Bl6 lungs from high oxygen induced lung injury.American journal of physiology. Cell physiology · 2026Article
- Macrophages of the heart: Homeostasis and disease.Biomedical journal · 2026Review
- Advances in nanomaterials for the diagnosis and treatment of ischemic heart disease.Discover nano · 2026Review
- Dynamic microRNA Signatures as Biomarkers for Cardiac Ischemia and Remodeling.International journal of molecular sciences · 2026Article
- BMP1 inhibitor UK383367 improves MI-induced cardiac remodeling and fibrosis in mice via ameliorating macrophage polarization and mitochondrial dysfunction.Acta pharmacologica Sinica · 2026Article
- Dynamic regulation and targeted interventions of macrophages in ischemia-reperfusion injury.Journal of advanced research · 2026Review
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- NF-Frontiers in cardiovascular medicine · 2026Review
10 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
2 authors at 1 institution in 1 country.
Funding
Abstract
The heart contains a population of resident macrophages that markedly expands following injury through recruitment of monocytes and through proliferation of macrophages. In myocardial infarction, macrophages have been implicated in both injurious and reparative responses. In coronary atherosclerotic lesions, macrophages have been implicated in disease progression and in the pathogenesis of plaque rupture. Following myocardial infarction, resident macrophages contribute to initiation and regulation of the inflammatory response. Phagocytosis and efferocytosis are major functions of macrophages during the inflammatory phase of infarct healing, and mediate phenotypic changes, leading to acquisition of an anti-inflammatory macrophage phenotype. Infarct macrophages respond to changes in the cytokine content and extracellular matrix composition of their environment and secrete fibrogenic and angiogenic mediators, playing a central role in repair of the infarcted heart. Macrophages may also play a role in scar maturation and may contribute to chronic adverse remodeling of noninfarcted segments. Single cell studies have revealed a remarkable heterogeneity of macrophage populations in infarcted hearts; however, the relations between transcriptomic profiles and functional properties remain poorly defined. This review manuscript discusses the fate, mechanisms of expansion and activation, and role of macrophages in the infarcted heart. Considering their critical role in injury, repair, and remodeling, macrophages are important, but challenging, targets for therapeutic interventions in myocardial infarction.
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What OpenQuestion holds
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.