Figure 4. Aggregate findings demonstrate no correlation between lymphangiogenesis and cardiac performance after MI.

(A) The ejection fraction data for all control animals [2 Flt4^fl/fl groups, and Vegfd^–/–; Vegfc^fl/fl animals, combined as Cre(–)] and animals genetically deficient in lymphangiogenesis [due to loss of pan-endothelial VEGFR3 (Flt4^fl/fl; Cdh5-Cre^ERT2), lymphatic endothelial VEGFR3 (Flt4^fl/fl; Prox1-Cre^ERT2), or the VEGFC and VEGFD ligands (Vegfd^–/–; Vegfc^fl/fl; R26-Cre^ERT2), combined as Cre(+)] are shown. Unweighted combination of all ejection fraction experiments for the Cre(–) (n = 30) and Cre(+) (n = 38) groups is shown. (B) The relationship between ejection fraction and the number of lymphatic endothelial cells detected in the infarct zone after MI using data from all studies is shown by dot plot. The overall correlation trendline and R² are shown. Cre(+) animals clustered to the left of the vertical dotted line, and Cre(–) animals clustered to the right. For A and B, littermates from Flt4^fl/fl; Cdh5-Cre^ERT2 experiments are denoted with a purple symbol (EC VEGFR3 cKO); littermates from Flt4^fl/fl; Prox1-Cre^ERT2 experiments are denoted with a white symbol (LEC VEGFR3 cKO); and littermates from Vegfd^–/–; Vegfc^fl/fl; R26-Cre^ERT2 experiments are denoted with a green symbol (VEGF-C cKO; VEGF-D KO). Female animals in A and B are shown as triangles, males are circles. Bar graphs represent mean ± SEM. Statistical comparison in A was made with a 2-tailed t test, and the trendline in B is a linear regression.