抗血管生成疗法是管理血管生成增加的疾病，如癌症、黄斑病和视网膜病的实用方法。考虑到对血管生成及其抑制所涉及的重要途径的了解存在基本缺陷以及现有抑制剂效率不足的情况，越来越多地关注新兴的治疗策略，旨在抑制病理性血管生成。血管生成是从现有血管形成新的血管网络；内皮细胞（ECs）是生理或病理情况下血管生成的主要参与者。在新的血管形成期间，从静止状态转换为高度迁移和增殖状态，即“血管生成切换”，由ECs、血管生成生长因子和其他信号驱动“代谢切换”。随着ECs的特性因改变周围环境而改变，在肿瘤微环境（TME）中似乎具有不同的代谢。因此，通过针对代谢途径来抑制病理性血管生成。在本综述中，我们旨在讨论正常和TME条件下的EC代谢通路，以验证使用新型疗法对其进行靶向治疗的适宜性。

Anti-angiogenic therapy is a practical approach to managing diseases with increased angiogenesis, such as cancer, maculopathies, and retinopathies. Considering the fundamental gaps in the knowledge of the vital pathways involved in angiogenesis and its inhibition and the insufficient efficiency of existing angiogenesis inhibitors, there is an increasing focus on the emergence of new therapeutic strategies aimed at inhibiting pathological angiogenesis. Angiogenesis is forming a new vascular network from existing vessels; endothelial cells (ECs), vascular lining cells, are the main actors of angiogenesis in physiological or pathological conditions. Switching from a quiescent state to a highly migratory and proliferative state during new vessel formation called "angiogenic switch" is driven by a "metabolic switch" in ECs, angiogenic growth factors, and other signals. As the characteristics of ECs change by altering the surrounding environment, they appear to have a different metabolism in a tumor microenvironment (TME). Therefore, pathological angiogenesis can be inhibited by targeting metabolic pathways. In the current review, we aim to discuss the EC metabolic pathways under normal and TME conditions to verify the suitability of targeting them with novel therapies.