ReviewTranslational research : the journal of laboratory and clinical medicine2018
Cardiac macrophage biology in the steady-state heart, the aging heart, and following myocardial infarction.
Review in Translational research : the journal of laboratory and clinical medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 247 papers, 1 of them a synthesis that pooled it.
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
247 citing papers in PubMed, 1 synthesis or guideline pooled it, 416 citations in OpenAlex.
- Reverse Onco-Cardiology: What Is the Evidence for Breast Cancer? A Systematic Review of the Literature.International journal of molecular sciences · 2023Pooled it
- Correlation Between Plasma Matrix Metalloproteinase-28 Levels and Severity of Calcific Aortic Valve Stenosis.Medical science monitor : international medical journal of experimental and clinical research · 2020Trial
- Myeloid Cell Expansion Propels Right Ventricular Dysfunction in HFpEF Through Sterile Inflammation.Circulation · 2026Article
- Cardiomyocyte-macrophage cross-talk reduces doxorubicin cardiotoxicity by polarizing macrophages via EV miR-142-3p/135a-5p.iScience · 2026Article
- Established and emerging roles of lysosomal dysfunction in cardiac aging.Nature cardiovascular research · 2026Review
- Review
- Metabolic regulation of macrophage polarization in myocardial infarction: from mechanisms to targeted therapies.Journal of translational medicine · 2026Review
- The Role of the Pentose Phosphate Pathway in Cardiovascular Diseases.Cardiovascular drugs and therapy · 2026Review
- Characterization of p16-positive stromal cells in age-related cardiac disorders.Journal of biochemistry · 2026Article
- Catestatin restores cardiac metabolic flexibility and enhances mitochondrial function.Communications biology · 2026Article
- Ferroptosis and macrophage polarization: mechanisms, interplay, and implications for medical applications.Cell death discovery · 2026Review
- A Versatile In Vitro Quantitative Assay for Macrophage Efferocytosis in Diverse Research Applications.Bio-protocol · 2026Article
- Morchella polysaccharide ameliorates myocardial infarction inflammation in mice through increasing gut microbiota-derived 12-HEPE.Acta pharmacologica Sinica · 2026Article
- Contributions of Biological Aging to Longitudinal Incidence and Dynamic Progression of Atrial Fibrillation: A Prospective Cohort Study.Reviews in cardiovascular medicine · 2026Article
- Mesaconate Alleviates Myocardial Ischemia/Reperfusion Injury and Cardiovascular Aging by Targeting GPR35 to Arrest Macrophage Inflammation.Inflammation · 2026Article
- Distinct immunometabolic signatures of type 1 versus type 2 diabetes in a murine model of myocardial infarction.Cardiovascular diabetology · 2026Article
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- Sequential polarization of macrophages: an immunomodulatory strategy for novel bone repair materials.Regenerative biomaterials · 2026Review
- The role of the bidirectional regulatory network between immune cells and stromal cells in cardiac repair and fibrosis following myocardial infarction.Frontiers in immunology · 2026Review
- Piezo1 Upregulation in Monocyte-Derived Macrophages Impairs Post-Myocardial Infarction Cardiac Repair via Defective Efferocytosis and Enhanced Ferroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
187 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 1 institution in 1 country.
Funding
Abstract
Macrophages play critical roles in homeostatic maintenance of the myocardium under normal conditions and in tissue repair after injury. In the steady-state heart, resident cardiac macrophages remove senescent and dying cells and facilitate electrical conduction. In the aging heart, the shift in macrophage phenotype to a proinflammatory subtype leads to inflammaging. Following myocardial infarction (MI), macrophages recruited to the infarct produce both proinflammatory and anti-inflammatory mediators (cytokines, chemokines, matrix metalloproteinases, and growth factors), phagocytize dead cells, and promote angiogenesis and scar formation. These diverse properties are attributed to distinct macrophage subtypes and polarization status. Infarct macrophages exhibit a proinflammatory M1 phenotype early and become polarized toward an anti-inflammatory M2 phenotype later post-MI. Although this classification system is oversimplified and needs to be refined to accommodate the multiple different macrophage subtypes that have been recently identified, general concepts on macrophage roles are independent of subtype classification. This review summarizes current knowledge about cardiac macrophage origins, roles, and phenotypes in the steady state, with aging, and after MI, as well as highlights outstanding areas of investigation.
Indexed as
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What Socratic 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 Socratic graph.