Vegfc, short for vascular endothelial growth factor C, is crucial for lymphatic and blood vessel development. It is involved in the VEGFC/D-VEGFR3/NRP2 axis, which plays a role in processes like tumor lymphangiogenesis and lymphatic metastasis [5]. Its expression can be regulated in various ways, and it has implications in numerous biological processes and diseases.

In mouse models, defective efferocytosis by macrophages after myocardial infarction led to reduced cardiac lymphangiogenesis and Vegfc expression. Mice deficient for myeloid Vegfc exhibited impaired ventricular contractility, adverse tissue remodeling, and reduced lymphangiogenesis, along with a defective inflammatory response [1]. In medulloblastoma cells, VEGFC negatively regulates cell growth and aggressiveness, with irradiation-resistant cells (high in VEGFC) losing migration and vessel-forming abilities [2]. In zebrafish, Vegfc expression in different cell types drives lymphatic development during heart development and regeneration, and overexpression enhances lymphatic expansion and scar resolution [3]. In renal cell carcinoma, VEGFC acts as a double-edged sword, with its role in tumor aggressiveness being more complex than previously thought [4].

In conclusion, Vegfc is essential for lymphatic and blood vessel development. Gene knockout and conditional knockout mouse models have revealed its role in cardiac injury repair, tumor growth regulation, and heart regeneration. These findings provide insights into the mechanisms of related diseases and potential therapeutic targets.