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Updated: Oct 16, 2025

Isolation of Human Lymphatic Endothelial Cells by Multi-parameter Fluorescence-activated Cell Sorting
Published on: May 1, 2015
Lymphatics in the broken heart
Ebba Bråkenhielm1, Yuguo Chen2, Yihai Cao3
1Normandy University, UniRouen, Inserm (Institut National de la Santé et de la Recherche Médicale) UMR1096 (EnVI Laboratory), FHU CARNAVAL, Rouen, France.
Insights
New research shows that promoting new lymphatic vessel growth in the heart after myocardial infarction (MI) does not improve cardiac function or reduce infarct expansion. This finding impacts therapeutic strategies for heart disease.
Area of Science:
- Cardiovascular Biology
- Lymphatic Research
- Myocardial Infarction Models
Background:
- Cardiac lymphatics are a potential therapeutic target for cardiovascular diseases, particularly after myocardial infarction (MI), to reduce edema and inflammation.
- Current therapeutic strategies often involve vascular endothelial growth factor C (VEGF-C) delivery, but the direct impact of cardiac lymphatic expansion on beneficial effects is unclear.
Purpose of the Study:
- To investigate the acute functional consequences of endogenous cardiac lymphangiogenesis within the infarct zone following MI in mice.
- To clarify the role of infarct lymphangiogenesis in left ventricular remodeling and function after MI.
Main Methods:
- Utilized complementary genetic mouse models to compare outcomes in the presence and absence of infarct lymphangiogenesis.
- Assessed infarct expansion, left ventricular dilation, and cardiac function post-MI.
Main Results:
- Cardiac lymphangiogenesis in the infarct zone after MI did not affect infarct expansion.
- Left ventricular dilation and overall cardiac function post-MI remained unchanged regardless of infarct lymphangiogenesis.
Conclusions:
- The study suggests that infarct lymphangiogenesis has no acute functional impact on cardiac remodeling or function after myocardial infarction in mice.
- These findings are crucial for refining research in cardiac lymphatics and guiding future clinical translation for ischemic heart disease treatment.
Abstract:
Cardiac lymphatics have emerged as a therapeutic target in cardiovascular diseases to limit myocardial edema and inflammation, notably after myocardial infarction (MI). While most experimental therapeutic approaches have focused on vascular endothelial growth factor C (VEGF-C) delivery, it remains uncertain to what degree the beneficial cardiac effects are related to lymphatic expansion in the heart. In this issue of the JCI, Keller, Lim, et al. reexamined the acute functional impact of endogenous cardiac lymphangiogenesis in the infarct zone after MI in mice. Their data, obtained by elegant comparisons of several complementary genetic mouse models, indicate that infarct expansion and left ventricular dilation and function after MI are unaffected by infarct lymphangiogenesis. This Commentary places the results into the context of previous findings. We believe these data will help further advance the research field of cardiac lymphatics to guide better clinical translation and benefit patients with ischemic heart disease.
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