ArticleeLife2024
Resident and recruited macrophages differentially contribute to cardiac healing after myocardial ischemia.
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Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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28citing papers in PubMed, 1 pooled it
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it.
- SIRT3 in post-myocardial infarction macrophage reprogramming: linking mitochondrial fitness to inflammation resolution and repair.Frontiers in immunology · 2026Pooled it
- Targeting NR4A1 (Nur77) in Macrophage Polarization: Molecular Mechanisms and Translational Prospects for Cardiac Repair After Myocardial Infarction.International journal of molecular sciences · 2026Review
- Selective expansion of cardiac macrophage subtypes distinguishes their functional roles in disease and homeostasis.The Journal of clinical investigation · 2026Article
- Depletion and replacement of tissue-resident macrophages in mice with germ-line deletion of a conserved enhancer in the Csf1r locus.Development (Cambridge, England) · 2026Article
- Myocardial Immune Niches in Homeostasis and Inflammation.Immunological reviews · 2026Review
- Epicardial Contributions to Fibro-Inflammatory Signaling in a Pkp2-Deficient Arrhythmogenic Cardiomyopathy Model.Circulation. Heart failure · 2026Article
- Algorithm-based quantification of tissue vascularization in immunohistochemical stainings of tissue sections.Scientific reports · 2026Article
- Organ-Specific and Conserved Regulatory Logic Orchestrates Gene Expression in the Embryonic Mesothelium.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- SAMHD1 promotes cardiac repair post myocardial infarction by targeting NR4a1 to regulate macrophage metabolic reprogramming.Journal of advanced research · 2026Article
- Macrophage-enriched HMOX1 is an ischemia-reperfusion-responsive marker in the heart.Journal of thoracic disease · 2026Article
- Interstitial cells and arrhythmia.American journal of physiology. Cell physiology · 2026Review
- Intense light mitigates hypoxia-induced right ventricular remodeling and dysfunction through reducing inflammation associated with PF4Genes & diseases · 2026Article
- Notch-1 in macrophages promoted the ischemia-reperfusion via modulating EZH2/HSF1/BRD4/SIRPα/SHP2 induced ROS and apoptosis in cardiomyocyte.Scientific reports · 2026Article
- The immune-cardiovascular metabolic circuitry in myocardial ischemia-reperfusion injury: from metabolic signal release to spatiotemporal reprogramming.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
- Macrophage polarization in ischemia-reperfusion injury: from molecular mechanisms to therapeutic strategies.Frontiers in immunology · 2026Review
- Administration of Single or Repeated Doses of CDCs in a Swine Model of Reperfused Myocardial Infarction: Magnetic Resonance and Proteomics Evaluation.International journal of molecular sciences · 2025Article
- Article
- Inhibition of Macrophage ARID3A Alleviates Myocardial Ischemia-Reperfusion Injury After Heart Transplantation by Reducing THBS1/CD47 Signaling-Mediated Neutrophil Extracellular Traps Formation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The spatial and temporal activation of macrophages during fibrosis.Nature reviews. Immunology · 2025Review
Corrections and comments
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Authors and funding
26 authors.
Tobias WeinbergerMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.ORCID https://orcid.org/0000-0003-0024-020X
Messerer DeniseMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.
Markus JoppichLFE Bioinformatik, Department of Informatics, Ludwig Maximilian University, Munich, Germany.ORCID https://orcid.org/0000-0002-6665-8951
Maximilian FischerMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.ORCID https://orcid.org/0000-0001-9172-3316
Clarisabel Garcia RodriguezInstitut Pasteur, Unité Macrophages et Développement de l'Immunité, Département de Biologie du Développement et Cellules Souches, Paris, France.
Konda KumaraswamiMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.
Vanessa WimmlerMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.
Sonja AblingerMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.
Saskia RäuberMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.ORCID https://orcid.org/0000-0001-8901-5572
Jiahui FangMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.
Lulu LiuMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.
Wing Han LiuMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.
Julia WinterhalterMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.
Johannes LichtiMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.
Lukas ThomasMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.
Dena EsfandyariDZHK (German Centre for Cardiovascular Research), Partner site Munich Heart Alliance, Munich, Germany.ORCID https://orcid.org/0000-0001-8732-1461
Guelce PercinImmunology of Aging, Leibniz-Institute on Aging - Fritz-Lipmann-Institute (FLI), Jena, Germany.
Sandra MatinArea of Cell & Developmental Biology, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.
Andrés HidalgoArea of Cell & Developmental Biology, Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.
Claudia WaskowImmunology of Aging, Leibniz-Institute on Aging - Fritz-Lipmann-Institute (FLI), Jena, Germany.
Stefan EngelhardtDZHK (German Centre for Cardiovascular Research), Partner site Munich Heart Alliance, Munich, Germany.ORCID https://orcid.org/0000-0001-5378-8661
Andrei TodicaDepartment of Nuclear Medicine, Ludwig Maximilian University, Munich, Germany.
Ralf ZimmerLFE Bioinformatik, Department of Informatics, Ludwig Maximilian University, Munich, Germany.
Clare PridansSimons Initiative for the Developing Brain, Centre for Discovery Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom.ORCID https://orcid.org/0000-0001-9423-557X
Elisa Gomez PerdigueroInstitut Pasteur, Unité Macrophages et Développement de l'Immunité, Département de Biologie du Développement et Cellules Souches, Paris, France.
Christian SchulzMedical Clinic I., Department of Cardiology, University Hospital, Ludwig Maximilian University, Munich, Germany.ORCID https://orcid.org/0000-0002-8149-0747
Funding
Deutsche Forschungsgemeinschaft SCHU 2297/1-1Deutsche Forschungsgemeinschaft SFB 1123 project A07Deutsche Forschungsgemeinschaft SFB 1123 project Z02Deutsche Forschungsgemeinschaft SFB TRR332, project A06Deutsches Zentrum für Herz-Kreislaufforschung 81X2600252Deutsches Zentrum für Herz-Kreislaufforschung 81X2600256Deutsches Zentrum für Herz-Kreislaufforschung 81Z0600204European Society of Cardiology Research Grant 2021
Abstract
Cardiac macrophages are heterogenous in phenotype and functions, which has been associated with differences in their ontogeny. Despite extensive research, our understanding of the precise role of different subsets of macrophages in ischemia/reperfusion (I/R) injury remains incomplete. We here investigated macrophage lineages and ablated tissue macrophages in homeostasis and after I/R injury in a CSF1R-dependent manner. Genomic deletion of a fms-intronic regulatory element (FIRE) in the
Indexed as
MacrophagesReceptors, Granulocyte-Macrophage Colony-Stimulating FactorAnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLMyocardial InfarctionMyocardial IschemiaMyocardial Reperfusion InjuryMyocardiumCsf1r protein, mouseReceptors, Granulocyte-Macrophage Colony-Stimulating Factordevelopmental biologyimmunologyinflammationmacrophagemousemyocardial infarction
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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.