Our results showed that although cardiac systolic function (LVFE and FS) was reduced in the HF model along with pulmonary edema, these pressure-overload-induced decreases in cardiac systolic function were reversed by XML stimulation via a mechanism involving the ERK1/2, AKT/GSK3β and GATA4 signaling pathways. The gene discussed is MAPK3; the disease is hydrops fetalis.