ArticleScientific reports2021
Cardiac macrophage subsets differentially regulate lymphatic network remodeling during pressure overload.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 46 citations in OpenAlex.
- Cardiac lymphatic dysfunction and repair in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- Myocardial Immune Niches in Homeostasis and Inflammation.Immunological reviews · 2026Review
- SIV infection induces aging-like alterations in cardiac cellularity and macrophage populations of rhesus macaques.Journal of leukocyte biology · 2026Article
- Cardiac Lymphatic Dysfunction in Heart Failure: A New Paradigm for Congestion, Inflammation, and Therapy.Medical sciences (Basel, Switzerland) · 2026Review
- Hyaluronan in cardiac disease: implications for the extracellular matrix beyond collagen.American journal of physiology. Heart and circulatory physiology · 2026Review
- Cardiac lymphatics: functional plasticity in development, disease, and precision-targeted therapies.Basic research in cardiology · 2026Review
- The role of the cardiac lymphatic system in heart failure "reverse remodeling": from developmental signals to druggable targets.Frontiers in immunology · 2026Review
- Normal cardiac lymphatics and their mimics.American journal of physiology. Heart and circulatory physiology · 2026Article
- Molecular determinants of cardiac lymphatic dysfunction in a chronic pressure-overload model.EMBO molecular medicine · 2026Article
- The role of macrophages in cardiac diseases: a review of the origins, functional diversity, and therapeutic potential.Frontiers in immunology · 2026Review
- Molecular Mechanisms and Therapeutic Strategies Targeting Cardiac Lymphangiogenesis in Heart Failure.Cardiovascular toxicology · 2025Review
- Crosstalk between lymphatic system and synovial inflammatory cells in osteoarthritis: molecular mechanisms and potential cell-based therapies.Journal of translational medicine · 2025Review
- Lymph Node-Targeted Cyclosporine A Alleviates Myocarditis in Lupus Mice by Inhibiting CD68+ Macrophage-Driven Lymphangiogenesis.Materials today (Kidlington, England) · 2025Article
- Cardiac macrophage: Insights from murine models to translational potential for human studies.Journal of molecular and cellular cardiology · 2025Review
- Leukocyte-lymphatic intersections during cardiac inflammation.Journal of molecular and cellular cardiology · 2025Review
- Research trends and hotspots of the applications of single-cell RNA sequencing in cardiovascular diseases: a bibliometric and visualized study.Annals of medicine and surgery (2012) · 2024Review
- Cardiac lymphatics undergo distinct remodeling during hypertrophic and nonhypertrophic pregnancy.American journal of physiology. Heart and circulatory physiology · 2024Article
- Disease-Specific Alteration of Cardiac Lymphatics: A Review from Animal Disease Models to Clinics.International journal of molecular sciences · 2024Review
- Single-cell transcriptomics reveals writers of RNA modification-mediated immune microenvironment and cardiac resident Macro-MYL2 macrophages in heart failure.BMC cardiovascular disorders · 2024Article
- The Efficacy of Risk Factor Modification Compared to NADJACC. Basic to translational science · 2024Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The lymphatic network of mammalian heart is an important regulator of interstitial fluid compartment and immune cell trafficking. We observed a remodeling of the cardiac lymphatic vessels and a reduced lymphatic efficiency during heart hypertrophy and failure induced by transverse aortic constriction. The lymphatic endothelial cell number of the failing hearts was positively correlated with cardiac function and with a subset of cardiac macrophages. This macrophage population distinguished by LYVE-1 (Lymphatic vessel endothelial hyaluronic acid receptor-1) and by resident macrophage gene expression signature, appeared not replenished by CCR2 mediated monocyte infiltration during pressure overload. Isolation of macrophage subpopulations showed that the LYVE-1 positive subset sustained in vitro and in vivo lymphangiogenesis through the expression of pro-lymphangiogenic factors. In contrast, the LYVE-1 negative macrophage subset strongly expressed MMP12 and decreased the endothelial LYVE-1 receptors in lymphatic endothelial cells, a feature of cardiac lymphatic remodeling in failing hearts. The treatment of mice with a CCR2 antagonist during pressure overload modified the proportion of macrophage subsets within the pathological heart and preserved lymphatic network from remodeling. This study reports unknown and differential functions of macrophage subpopulations in the regulation of cardiac lymphatic during pathological hypertrophy and may constitute a key mechanism underlying the progression of heart failure.
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