- Academic Editor
-
-
-
Background: The dilation of lymphatic vessels plays a critical role in
maintaining heart function, while a lack thereof could contribute to heart
failure (HF), and subsequently to an acute myocardial infarction (AMI).
Macrophages participate in the induction of lymphangiogenesis by secreting
vascular endothelial cell growth factor C (VEGF-C), although the precise
mechanism remains unclear. Methods: Intramyocardial injections of
adeno-associated viruses (AAV9) to inhibit the expression of VEGFR3
(VEGFR3 shRNA) or promote the expression of VEGFR3
(VEGFR3 ORF) in the heart; Myh6-mCherry B6 D2-tg mice and flow cytometry
were used to evaluate the number of myocellular debris in the mediastinal lymph
nodes; fluorescence staining and qPCR were used to evaluate fluorescence
analysis; seahorse experiment was used to evaluate the level of glycolysis of
macrophages; Lyz2