Angiogenesis and lymphangiogenesis contribute to the development of endometriosis. We recently reported that thromboxane A₂ (TXA₂) receptor signaling involves in angiogenesis in critical limb ischemia and lymphangiogenesis in inflamed diaphragm. In the present study, using wild-type mice (WT) and thromboxane prostanoid receptor (TP) knockout mice (TPKO), we examined whether TP signaling plays a role in the growth of endometriosis by angiogenic responses. Ectopic endometriosis model was created by transplantation of endometrial tissue fragments from donor mice (WT or TPKO) into the peritoneal wall of host mice (WT or TPKO). The implant sizes and density of blood and lymphatic vessels in the TPKO implants from host TPKO (TPKO→TPKO) were increased as compared with the WT→WT. The mRNA levels of markers for blood (CD31) and lymphatic vessels (LYVE-1) and of growth factors for angiogenesis (VEGF-A) and lymphangiogenesis (VEGF-C/D) in the TPKO→TPKO were higher than those in the WT→WT. Immunostaining showed that TP was expressed in F4/80-positive macrophages, but not in blood and lymphatic vessels in endometriosis lesions. The levels of M2 macrophage-related genes were higher in the TPKO→TPKO than in the WT→WT, while no statistically significant difference in M1 macrophage-related genes was observed. These results suggest that TP signaling inhibits the growth of endometriosis by reducing angiogenesis and lymphangiogenesis.