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普罗波通过激活细胞内网膜应激来抑制TFAP2C驱动的VEGFA转录来减弱血管生成
Fan Yang1,2, Yi Liu1,2, Hui Li3
1Departmentof Anesthesiology, Shanghai Cancer Center, Fudan University, Shanghai, 200032, China.
Apoptosis : an international journal on programmed cell death
|January 12, 2026
概括
麻醉剂普罗波福 (propofol) 通过诱导细胞内网膜应激来抑制血管生成,从而抑制转录因子TFAP2C,这是VEGFA的关键调节者. 这一发现为血管生成相关疾病提供了新的治疗点.
科学领域:
- 分子生物学分子生物学
- 细胞生物学 细胞生物学
- 药理学 药理学是指药理学的学科.
背景情况:
- 麻醉引起的血液动力学变化会影响血管微环境和内皮细胞行为.
- 普罗波在瘤血管生成中的作用已知,但其对非恶性血管生成的影响尚不清楚.
- 糖尿病视网膜病,病和冠状动脉心脏病涉及异常血管生成.
研究的目的:
- 为了研究醇对血管内皮生长因子A (VEGFA) 介导的血管生成的影响.
- 阐明波对血管生成影响的分子机制.
- 确定潜在的治疗点来管理血管新生相关的疾病.
主要方法:
- 进行了体外和体内研究,以评估普罗波对血管生成的影响.
- 分析了包括PERK和eIF2α酸化在内的内等质网膜 (ER) 应激通路.
- 研究了转录因子AP-2 (TFAP2C) 与VEGFA促进物的相互作用.
主要成果:
- 普罗波通过激活PERK和eIF2α酸化来诱导ER压力.
- 这种压力抑制了TFAP2C的翻译,TFAP2C是内皮功能关键的转录因子.
- TFAP2C直接与VEGFA促进体结合,激活其转录并促进VEGFA/VEGFR2依赖的血管生成.
结论:
- 普罗波通过ER压力和随后的TFAP2C的抑制来抑制VEGFA介导的血管生成.
- TFAP2C被确定为VEGFA的新型转录调节剂.
- 这些发现提供了对普罗波福的药理作用的见解,并建议针对VEGFA介导血管生成的新治疗策略.
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