肿瘤血管与正常血管在功能和形态上不同，这导致了肿瘤微环境中的缺氧（TME）。先前的抗血管生成治疗在癌症免疫治疗方面取得了一定的改善。然而，抗血管生成治疗只对少数患者有益，并引起了许多副作用。因此，仍然需要开发一种新方法来影响肿瘤血管生成。血管内皮细胞（ECs）表面上表达的CD93受体及其自然配体MMRN2和IGFBP7现被认为是抗血管生成治疗的潜在靶标，因为最近的研究报道称，抗CD93可以使肿瘤血管正常化而不影响正常血管。在这里，我们回顾了关于CD93、IGFBP7和MMRN2在血管生成中的作用的最新研究。我们着重揭示IGFBP7-CD93和MMRN2-CD93之间的相互作用以及CD93、IGFBP7和MMRN2在血管生成过程中影响的信号级联。我们还回顾了关于CD93、IGFBP7和MMRN2表达及其与临床因素的关系的回顾性研究。总之，CD93是使肿瘤血管正常化的有希望的靶点。©2023 BioMed Central Ltd，Springer Nature的一部分。

The tumor vasculature was different from the normal vasculature in both function and morphology, which caused hypoxia in the tumor microenvironment (TME). Previous anti-angiogenesis therapy had led to a modest improvement in cancer immunotherapy. However, antiangiogenic therapy only benefitted a few patients and caused many side effects. Therefore, there was still a need to develop a new approach to affect tumor vasculature formation. The CD93 receptor expressed on the surface of vascular endothelial cells (ECs) and its natural ligands, MMRN2 and IGFBP7, were now considered potential targets in the antiangiogenic treatment because recent studies had reported that anti-CD93 could normalize the tumor vasculature without impacting normal blood vessels. Here, we reviewed recent studies on the role of CD93, IGFBP7, and MMRN2 in angiogenesis. We focused on revealing the interaction between IGFBP7-CD93 and MMRN2-CD93 and the signaling cascaded impacted by CD93, IGFBP7, and MMRN2 during the angiogenesis process. We also reviewed retrospective studies on CD93, IGFBP7, and MMRN2 expression and their relationship with clinical factors. In conclusion, CD93 was a promising target for normalizing the tumor vasculature.© 2023. BioMed Central Ltd., part of Springer Nature.