ReviewFrontiers in cardiovascular medicine2019
Immunometabolism of Phagocytes and Relationships to Cardiac Repair.
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 34 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
34 citing papers in PubMed.
- Dynamic regulation of the 'mitochondria‑immune axis' in myocardial infarction: Molecular mechanisms driving macrophage polarization through energy metabolism disorders (Review).Molecular medicine reports · 2026Review
- Cardiometabolic reprogramming in pulmonary arterial hypertension: Implications for right ventricular dysfunction and therapeutic strategies.Chinese herbal medicines · 2026Review
- SAMHD1 promotes cardiac repair post myocardial infarction by targeting NR4a1 to regulate macrophage metabolic reprogramming.Journal of advanced research · 2026Article
- Review
- Metabolism Serves as a Bridge Between Cardiomyocytes and Immune Cells in Cardiovascular Diseases.Cardiovascular drugs and therapy · 2025Review
- Haematometabolism rewiring in atherosclerotic cardiovascular disease.Nature reviews. Cardiology · 2025Review
- Proteomic evaluation of the thrombosis-inflammation interplay in STEMI with MVO.BMC cardiovascular disorders · 2025Article
- Development and Validation of the Systemic Inflammatory Response Index-Based Nomogram for Predicting Short-Term Adverse Events in Patients With Acute Uncomplicated Type B Aortic Intramural Hematoma.Journal of inflammation research · 2025Article
- Major cell types in the coronary thrombosis of acute myocardial infarction patients revealed by scRNA-seq.Clinical and translational medicine · 2025Article
- Mitochondrial transplantation following cardiopulmonary resuscitation improves neurological function in rats by inducing M2-type MG/MΦ polarization.Journal of translational medicine · 2024Article
- Myeloid Cells in Myocardial Ischemic Injury: The Role of the Macrophage Migration Inhibitory Factor.Life (Basel, Switzerland) · 2024Review
- Cardiac macrophage metabolism in health and disease.Trends in endocrinology and metabolism: TEM · 2024Review
- The effect of macrophages and their exosomes in ischemic heart disease.Frontiers in immunology · 2024Review
- Cardiac fibrogenesis: an immuno-metabolic perspective.Frontiers in physiology · 2024Review
- Integration of Microarray Data and Single-Cell Sequencing Analysis to Explore Key Genes Associated with Macrophage Infiltration in Heart Failure.Journal of inflammation research · 2024Article
- Bone marrow adipocytes fuel emergency hematopoiesis after myocardial infarction.Nature cardiovascular research · 2023Article
- Metabolic mechanisms in physiological and pathological cardiac hypertrophy: new paradigms and challenges.Nature reviews. Cardiology · 2023Review
- Effects of Glucose Levels on Inflammation and Amino Acid Utilization in Lipopolysaccharide-Induced Bovine Mammary Epithelial Cells.Animals : an open access journal from MDPI · 2023Article
- Inflammation in Myocardial Ischemia/Reperfusion Injury: Underlying Mechanisms and Therapeutic Potential.Antioxidants (Basel, Switzerland) · 2023Review
- Mitochondrial dysfunction in macrophages promotes inflammation and suppresses repair after myocardial infarction.The Journal of clinical investigation · 2023Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Cardiovascular disease remains the leading cause of death worldwide. Myocardial ischemia is a major contributor to cardiovascular morbidity and mortality. In the case of acute myocardial infarction, subsequent cardiac repair relies upon the acute, and coordinated response to injury by innate myeloid phagocytes. This includes neutrophils, monocytes, macrophage subsets, and immature dendritic cells. Phagocytes function to remove necrotic cardiomyocytes, apoptotic inflammatory cells, and to remodel extracellular matrix. These innate immune cells also secrete cytokines and growth factors that promote tissue replacement through fibrosis and angiogenesis. Within the injured myocardium, macrophages polarize from pro-inflammatory to inflammation-resolving phenotypes. At the core of this functional plasticity is cellular metabolism, which has gained an appreciation for its integration with phagocyte function and remodeling of the transcriptional and epigenetic landscape. Immunometabolic rewiring is particularly relevant after ischemia and clinical reperfusion given the rapidly changing oxygen and metabolic milieu. Hypoxia reduces mitochondrial oxidative phosphorylation and leads to increased reliance on glycolysis, which can support biosynthesis of pro-inflammatory cytokines. Reoxygenation is permissive for shifts back to mitochondrial metabolism and fatty acid oxidation and this is ultimately linked to pro-reparative macrophage polarization. Improved understanding of mechanisms that regulate metabolic adaptations holds the potential to identify new metabolite targets and strategies to reduce cardiac damage through nutrient signaling.
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Registered trials
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