心梗后心肌病理性重构导致心衰，心脏淋巴管发挥将炎症细胞等引流从而减少对心肌负面影响的作用。阐明心梗后淋巴管重构的机制，维持淋巴管的功能完整，能够为心梗后心功能的改善提供进一步保障。研究发现ephrinB2- EphB4在淋巴管发育中发挥重要作用。另外ephrinB2与其配体EphB4结合后，在角膜疾病模型中也被证实可促进角膜淋巴管的重构。但ephrinB2-EphB4通路在成体心脏心梗后淋巴管重构是否发挥作用尚无研究报道。我们前期研究发现心梗后心脏淋巴管存在新生与重构，心肌外源性注射EphB4/Fc可以促进淋巴管重构，且与VEGFR3受体内吞相关。因此我们提出假设：ephrinB2-EphB4在心梗后心脏淋巴管重构的过程中作为VEGFR3内吞的重要促进因素，影响VEGFR3与VEGFC结合之后的PI3K-Akt-Rac1、mTOR和MAPK-Erk信号通路网，调节淋巴管重构，改善心功能。

Myocardial pathological remodeling after myocardial infarction leads to heart failure and the lymphatic vessels of the heart play a role in draining inflammatory cells to reduce negative effects on the myocardium. In light to the mechanism of lymphatic remodeling and above all understand how maintaining the functional integrity of lymphatic vessels exhibited evidence of further protection for the improvement of the tissue after the pathological insult. Our study found that ephrinB2-EphB4 played an important role in lymphatic development. In addition, ephrinB2 has been shown to promote corneal lymphatic remodeling in corneal disease models after binding to its ligand EphB4. Prior to date, there is no research report on whether the ephrinB2-EphB4 pathway plays a role in lymphatic remodeling after adult cardiac myocardial infarction. Our previous study found that there was neogenesis and active remodeling of cardiac lymphatic vessels after myocardial infarction. Exogenous injection of EphB4/Fc could promote lymphatic vessel remodeling and was associated with VEGFR3 receptor endocytosis. Therefore, we hypothesized that ephrinB2-EphB4 acts as an important promoter of VEGFR3 endocytosis during cardiac lymphangiogenesis after myocardial infarction, affecting PI3K-Akt-Rac1, mTOR and MAPK-Erk signaling pathways after VEGFR3 binds to VEGFC, thus regulating lymphatic vessel remodeling and improving cardiac function.