Luo Shiwen, Li Liu, Chen Huiqing, Wei Jingyue, Yang Dongmei
Key Laboratory of Vascular Biology and Translational Medicine, Medical School, Hunan University of Chinese Medicine, 410208 Changsha, Hunan, China.
College of Integrated Chinese and Western Medicine, Hunan University of Chinese Medicine, 410208 Changsha, Hunan, China.
Rev Cardiovasc Med. 2024 Nov 22;25(11):423. doi: 10.31083/j.rcm2511423. eCollection 2024 Nov.
Atherosclerosis (AS) is an important cause of morbidity and mortality in cardiovascular diseases such as coronary atherosclerotic heart disease and stroke. As the primary natural barrier between blood and the vessel wall, damage to vascular endothelial cells (VECs) is one of the initiating factors for the development of AS. VECs primarily use aerobic glycolysis for energy supply, but several diseases can cause altered glucose metabolism in VECs. Glucose metabolism reprogramming of VECs is the core event of AS, which is closely related to the development of AS. In this review, we review how glucose metabolism reprogramming of VECs promotes the development of AS by inducing VEC barrier dysfunction, autophagy, altering the inflammatory response, and proliferation of VECs, in the hopes of providing new ideas and discovering new targets for the prevention and treatment of AS.
动脉粥样硬化（AS）是冠心病和中风等心血管疾病发病和死亡的重要原因。作为血液与血管壁之间的主要天然屏障，血管内皮细胞（VECs）损伤是AS发生发展的起始因素之一。VECs主要通过有氧糖酵解提供能量，但多种疾病可导致VECs葡萄糖代谢改变。VECs葡萄糖代谢重编程是AS的核心事件，与AS的发生发展密切相关。在本综述中，我们探讨VECs葡萄糖代谢重编程如何通过诱导VEC屏障功能障碍、自噬、改变炎症反应和VECs增殖来促进AS的发生发展，以期为AS的防治提供新思路和发现新靶点。
