持续的肿瘤血管生成，即肿瘤细胞诱导和维持血管生长，是癌症的标志之一。恶性组织的血管化不仅有利于肿瘤的生长和转移，而且有助于免疫逃避。所有这些过程中的重要参与者是排列在血管腔侧的内皮细胞。在肿瘤血管系统中，这些细胞积极参与血管生成以及阻碍免疫细胞的招募。这是异常肿瘤微环境的结果，异常肿瘤微环境触发内皮细胞中的血管刺激和免疫抑制基因表达谱。近年来，很明显半乳糖凝集素构成了在肿瘤内皮细胞中表达的蛋白质家族。此外，已发现该聚糖结合蛋白家族的几个成员可以促进肿瘤血管生成并刺激免疫抑制。所有这些都表明半乳糖凝集素是潜在的治疗靶点，可以同时阻碍肿瘤血管生成并减轻免疫抑制。当前的综述提供了人类半乳糖凝集素蛋白家族的简要介绍。总结了有关内皮细胞中半乳糖凝集素表达和调节的当前知识。此外，还概述了内皮半乳糖凝集素在肿瘤血管生成和肿瘤免疫调节中发挥的作用。最后，讨论了未来研究工作应解决的一些突出问题。这将有助于充分了解内皮半乳糖凝集素对肿瘤进展的贡献，并利用内皮半乳糖凝集素进行癌症治疗。© 2024。作者。

Sustained tumor angiogenesis, i.e., the induction and maintenance of blood vessel growth by tumor cells, is one of the hallmarks of cancer. The vascularization of malignant tissues not only facilitates tumor growth and metastasis, but also contributes to immune evasion. Important players in all these processes are the endothelial cells which line the luminal side of blood vessel. In the tumor vasculature, these cells are actively involved in angiogenesis as well in the hampered recruitment of immune cells. This is the result of the abnormal tumor microenvironment which triggers both angiostimulatory and immune inhibitory gene expression profiles in endothelial cells. In recent years, it has become evident that galectins constitute a protein family that is expressed in the tumor endothelium. Moreover, several members of this glycan-binding protein family have been found to facilitate tumor angiogenesis and stimulate immune suppression. All this has identified galectins as potential therapeutic targets to simultaneously hamper tumor angiogenesis and alleviate immune suppression. The current review provides a brief introduction in the human galectin protein family. The current knowledge regarding the expression and regulation of galectins in endothelial cells is summarized. Furthermore, an overview of the role that endothelial galectins play in tumor angiogenesis and tumor immunomodulation is provided. Finally, some outstanding questions are discussed that should be addressed by future research efforts. This will help to fully understand the contribution of endothelial galectins to tumor progression and to exploit endothelial galectins for cancer therapy.© 2024. The Author(s).