FLT4 and cardiac hypertrophy: Under physiological conditions, exercise-induced myocardial hypertrophy is dependent on parallel lymphangiogenesis via activation of VEGF receptor 3 (VEGFR3).170 Pharmacological blockade of VEGFR3 resulted in lower secretion of IGF-1 and reelin, both of which seem to mediate crosstalk between lymphatic endothelial cells and cardiomyocytes.