ArticleThe Journal of clinical investigation2022
Macrophage-produced VEGFC is induced by efferocytosis to ameliorate cardiac injury and inflammation.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 110 papers.
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Who cites it
110 citing papers in PubMed, 145 citations in OpenAlex.
- General View of Arachidonic Acid (AA) Metabolism.Reviews of physiology, biochemistry and pharmacology · 2027Review
- Cardiac lymphatic dysfunction and repair in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- LncRNAiScience · 2026Article
- The crosstalk between lymphatic endothelial cells and immune cells in Physiological and Pathological conditions.Cellular and molecular life sciences : CMLS · 2026Review
- Cardiac Lymphatic Dysfunction in Heart Failure: A New Paradigm for Congestion, Inflammation, and Therapy.Medical sciences (Basel, Switzerland) · 2026Review
- Review
- Macrophage Efferocytosis in Heart.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- MARCH2 prevents doxorubicin-induced cardiomyopathy by stabilizing NR1H2 and promoting clearance of apoptotic cardiomyocytes.Nature communications · 2026Article
- Macrophage efferocytosis in cardiovascular disease: mechanisms and therapeutic implications.ImmunoHorizons · 2026Review
- Cellular and molecular signals of cardiac wound healing after myocardial infarction.American journal of physiology. Heart and circulatory physiology · 2026Review
- More Than a Cleanup Crew: The Expanding Biology of Efferocytosis.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Transcriptome and m6A epitranscriptome profiling reveal CCL20 as a key mediator of inflammation in Staphylococcus aureus-induced bovine mastitis.BMC microbiology · 2026Article
- Different forms of cardiomyocyte death in post-myocardial infarction ventricular remodeling: mechanisms and therapeutic strategies.Frontiers in cardiovascular medicine · 2026Review
- Efferocytosis in myocardial infarction: the regulatory core from inflammation resolution to cardiac repair.Frontiers in immunology · 2026Review
- The role of the cardiac lymphatic system in heart failure "reverse remodeling": from developmental signals to druggable targets.Frontiers in immunology · 2026Review
- Prognostic Value of Systemic Inflammatory Indices in Hospitalized Patients with HFrEF: A Multicenter Retrospective Cohort Study.International journal of general medicine · 2026Article
- Single-cell RNA sequencing pseudobulk analysis and machine learning identify candidate biomarkers for ischemic cardiomyopathy.Frontiers in cardiovascular medicine · 2026Article
- 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
- The neuroimmune axis in cardiovascular disease: from immune activation to inflammatory resolution.Frontiers in immunology · 2026Review
- From marrow memory to adverse ventricular remodeling: trained immunity after myocardial infarction.Frontiers in immunology · 2026Review
50 more citing papers are in PubMed but not listed here.
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Authors and funding
10 authors at 4 institutions in 2 countries.
Funding
Abstract
Clearance of dying cells by efferocytosis is necessary for cardiac repair after myocardial infarction (MI). Recent reports have suggested a protective role for vascular endothelial growth factor C (VEGFC) during acute cardiac lymphangiogenesis after MI. Here, we report that defective efferocytosis by macrophages after experimental MI led to a reduction in cardiac lymphangiogenesis and Vegfc expression. Cell-intrinsic evidence for efferocytic induction of Vegfc was revealed after adding apoptotic cells to cultured primary macrophages, which subsequently triggered Vegfc transcription and VEGFC secretion. Similarly, cardiac macrophages elevated Vegfc expression levels after MI, and mice deficient for myeloid Vegfc exhibited impaired ventricular contractility, adverse tissue remodeling, and reduced lymphangiogenesis. These results were observed in mouse models of permanent coronary occlusion and clinically relevant ischemia and reperfusion. Interestingly, myeloid Vegfc deficiency also led to increases in acute infarct size, prior to the amplitude of the acute cardiac lymphangiogenesis response. RNA-Seq and cardiac flow cytometry revealed that myeloid Vegfc deficiency was also characterized by a defective inflammatory response, and macrophage-produced VEGFC was directly effective at suppressing proinflammatory macrophage activation. Taken together, our findings indicate that cardiac macrophages promote healing through the promotion of myocardial lymphangiogenesis and the suppression of inflammatory cytokines.
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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.