VEGFC and myocardial infarction: In the acute and chronic phases of repair and recovery after mouse MI, therapeutic lymphangiogenesis via AAV-VEGF-CC156S gene delivery has prevented cardiac lymphatic reduction, and limited cardiac inflammation and dysfunction, but conversely, AAV-sVEGFR-3 (soluble VEGFR-3, VEGF-C/VEGF-D trap) has inhibited infarct lymphangiogenesis and reduced T-cell infiltration and deleterious cardiac remodeling [13].