ArticleScientific reports2018
Downregulation of VEGFR3 signaling alters cardiac lymphatic vessel organization and leads to a higher mortality after acute myocardial infarction.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 59 citations in OpenAlex.
- Cardiac lymphatic dysfunction and repair in cardiovascular disease.Nature reviews. Cardiology · 2026Review
- Simultaneous 3-D Adiabatic TNMR in biomedicine · 2026Article
- Single-cell and spatial transcriptomic analyses reveal the dynamic transcript profiles of myocardial lymphangiogenesis post-myocardial infarction.Chinese medical journal · 2026Article
- Targeting lymphatic vessels enhances bone regeneration by augmenting osteoclast activity in mouse models of amputation.The Journal of clinical investigation · 2026Article
- The role of the cardiac lymphatic system in heart failure "reverse remodeling": from developmental signals to druggable targets.Frontiers in immunology · 2026Review
- Molecular Mechanisms and Therapeutic Strategies Targeting Cardiac Lymphangiogenesis in Heart Failure.Cardiovascular toxicology · 2025Review
- Capturing Acute and Subchronic Myocardial Infarct by MRI Rotating Frame Relaxation Times in Mice In and Ex Vivo.NMR in biomedicine · 2025Article
- sVEGFR3 alleviates myocardial ischemia/reperfusion injury through regulating mitochondrial homeostasis and immune cell infiltration.Apoptosis : an international journal on programmed cell death · 2025Article
- Tissue-Engineered Therapeutics for Lymphatic Regeneration: Solutions for Myocardial Infarction and Secondary Lymphedema.Advanced healthcare materials · 2025Review
- Disease-Specific Alteration of Cardiac Lymphatics: A Review from Animal Disease Models to Clinics.International journal of molecular sciences · 2024Review
- Decorin suppresses tumor lymphangiogenesis: A mechanism to curtail cancer progression.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Lymphangiogenesis: A new strategy for heart disease treatment (Review).International journal of molecular medicine · 2024Review
- Angiogenesis-An Emerging Role in Organ Fibrosis.International journal of molecular sciences · 2023Review
- Mechanisms regulating vascular and lymphatic regeneration in the heart after myocardial infarction.The Journal of pathology · 2023Review
- The Lymphatic Vasculature in Cardiac Development and Ischemic Heart Disease.Circulation research · 2023Review
- Lymphatic insufficiency leads to distinct myocardial infarct content assessed by magnetic resonance TScientific reports · 2023Article
- Role of Lymphangiogenesis in Cardiac Repair and Regeneration.Methodist DeBakey cardiovascular journal · 2023Review
- The ebb and flow of cardiac lymphatics: a tidal wave of new discoveries.Physiological reviews · 2023Review
- The role of lymphangiogenesis in cardiovascular diseases and heart transplantation.Heart failure reviews · 2022Review
- Lymphangiogenesis contributes to exercise-induced physiological cardiac growth.Journal of sport and health science · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heart has a wide lymphatic network but the importance of cardiac lymphatic system in heart diseases has remained unclear. Vascular Endothelial Growth Factor Receptor 3 (VEGFR3) is a key molecule in the development and maintenance of cardiac lymphatic vessels. Here we characterized the role of VEGFR3 in healthy hearts and after myocardial infarction (MI) by using sVEGFR3 transgenic mice expressing a soluble decoy VEGFR3 under K14 promoter and Chy mice which have an inactivating mutation in the VEGFR3 gene. Cardiac lymphatic vessels were significantly dilated in the healthy hearts of sVEGFR3 mice when compared to controls. Lymphatic vessels formed large sheet-like structures in Chy mice. Attenuated VEGFR3 signaling led to a more severe MI predisposing to a significantly higher mortality in sVEGFR3 mice than in control mice. sVEGFR3 mice displayed intramyocardial hemorrhages in the infarcted area indicating hyperpermeability of the vasculature. Furthermore, novel MRI methods TRAFF2 and TRAFF4 and histological analysis revealed a modified structure of the fibrotic infarcted area in sVEGFR3 mice. In conclusion, the downregulation of VEGFR3 signaling modifies the structure of cardiac lymphatic network and causes vascular leakiness and increased mortality after MI.
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