血管内皮功能障碍和免疫细胞代谢编程在动脉样硬化的发展和侵袭中的作用
Guo Zhili1, Guan Zhimin1, Zhang Nenghua1
1Jiaxing Hospital of Traditional Chinese Medicine, Jiaxing University, Jiaxing, Zhejiang, China.
Frontiers in physiology
|September 19, 2025
概括
动脉样硬化涉及内皮功能障碍和免疫细胞代谢重编程之间的复杂相互作用. 了解这种动态是开发针对血管健康和炎症的有效疗法的关键.
科学领域:
- 心血管生物学 心血管生物学
- 免疫代谢过程中的免疫代谢.
- 动脉样硬化的发病因子
背景情况:
- 动脉样硬化 (AS) 的发病包括内皮功能障碍和免疫代谢障碍.
- 内皮细胞 (ECs) 转向有氧糖解 (Warburg效应) 并增殖,导致血管重塑.
- 免疫细胞通过代谢重编程适应AS微环境,增强炎症和脂质吸收.
研究的目的:
- 系统地分析血管内皮功能障碍和AS中的免疫代谢重编程之间的动态相互作用.
- 在这些过程的交叉点探索分子机制和治疗点.
- 为了解决AS治疗策略中的当前争议.
主要方法:
- 分子机制的系统审查和分析.
- 讨论内皮细胞和免疫细胞中的免疫代谢重编程.
- 探索动脉样硬化治疗的治疗点.
主要成果:
- 内皮功能障碍和免疫代谢障碍在AS病变发生过程中密切相关.
- 无论是EC细胞还是免疫细胞的代谢重编程都会导致AS的进展.
- 因果关系和协同效应需要进一步阐明.
结论:
- 针对内皮功能障碍和免疫代谢之间的相互作用,为动脉样硬化提供了新的治疗途径.
- 需要进一步的研究来澄清因果关系并优化治疗策略.
- 对这些相互作用的全面理解对于推进AS治疗至关重要.
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