ArticleThe American journal of pathology2007
Macrophage depletion impairs wound healing and increases left ventricular remodeling after myocardial injury in mice.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 298 papers, 1 of them a synthesis that pooled it.
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Who cites it
298 citing papers in PubMed, 1 synthesis or guideline pooled it, 537 citations in OpenAlex.
- Myocardial Immune Cells: The Basis of Cardiac Immunology.Journal of immunology (Baltimore, Md. : 1950) · 2023Pooled it
- Translational biology of human cardiac fibrosis.Nature cardiovascular research · 2026Review
- Fate-mapping infiltrating monocytes following experimental myocardial infarction reveals differentiation trajectories in the infarcted heart.The Journal of clinical investigation · 2026Article
- Emerging Roles for Metabolism in Myocardial Inflammation During Heart Failure.Immunological reviews · 2026Review
- Diabetes and Delayed Wound Healing: Molecular Mechanisms and Dermatological Interventions.International wound journal · 2026Review
- T Cell Receptor Repertoires Across the Continuum of Vascular, Myocardial, and Age-Related Diseases.Immunological reviews · 2026Review
- The Thoracic Lymphatic Vasculature: Interorgan Strategies to Achieve an Optimal Tissue Function.Comprehensive Physiology · 2026Review
- Kynurenic Acid/GPR35 Signaling Protects the Infarcted Heart by Suppressing Macrophage mtDNA-Triggered cGAS-STING Activation.Antioxidants (Basel, Switzerland) · 2026Article
- The Role of Phagocytic Cells in the Achilles Tendon.International journal of molecular sciences · 2026Review
- 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
- Machine Learning Integrates Bulk and Single-Nucleus RNA Sequence to Explore Apoptosis-Related Gene in Myocardial Infarction.Cardiovascular therapeutics · 2026Article
- Exercise-induced histone lactylation in monocyte-derived macrophages restores cardiac immune homeostasis and function in sepsis-induced cardiomyopathy.Nature communications · 2025Article
- Macrophage ITGAV is dispensable for post-infarction remodeling in mice and does not mediate fibronectin responses.Communications biology · 2025Article
- Inflammation-resolution signalling in cardiac repair, remodelling, and heart failure.European heart journal open · 2025Review
- Centers for Medical Countermeasures against Radiation Consortium: Past, Present, and Beyond.Radiation research · 2025Review
- SLAMF7 Restrains Pro-Inflammatory Macrophage Activation to Counteract Doxorubicin-Induced Cardiotoxicity.JACC. Basic to translational science · 2025Article
- WISP2/CCN5 revealed as a potential diagnostic biomarker for endometriosis based on machine learning and single-cell transcriptomic analysis.Functional & integrative genomics · 2025Article
- Klf9 promotes the repair of myocardial infarction by regulating macrophage recruitment and polarization.JCI insight · 2025Article
- Cardiomyocyte proliferation: Advances and insights in macrophage-targeted therapy for myocardial injury.Genes & diseases · 2025Review
238 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophages have been suggested to be beneficial for myocardial wound healing. We investigated the role of macrophages in myocardial wound healing by inhibition of macrophage infiltration after myocardial injury. We used a murine cryoinjury model to induce left ventricular damage. Infiltrating macrophages were depleted during the 1st week after cryoinjury by serial intravenous injections of clodronate-containing liposomes. After injury, the presence of macrophages, which secreted high levels of transforming growth factor-beta and vascular endothelial growth factor-A, led to rapid removal of cell debris and replacement by granulation tissue containing inflammatory cells and blood vessels, followed by myofibroblast infiltration and collagen deposition. In macrophage-depleted hearts, nonresorbed cell debris was still observed 4 weeks after injury. Secretion of transforming growth factor-beta and vascular endothelial growth factor-A as well as neovascularization, myofibroblast infiltration, and collagen deposition decreased. Moreover, macrophage depletion resulted in a high mortality rate accompanied by increased left ventricular dilatation and wall thinning. In conclusion, infiltrating macrophage depletion markedly impairs wound healing and increases remodeling and mortality after myocardial injury, identifying the macrophage as a key player in myocardial wound healing. Based on these findings, we propose that increasing macrophage numbers early after myocardial infarction could be a clinically relevant option to promote myocardial wound healing and subsequently to reduce remodeling and heart failure.
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