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细胞内膜网膜应激驱动单细胞细胞中的VEGF基因表达.

Fatemah Bahman1, Taha Nadeem2, Abdulrahman Alayyaf3

  • 1Immunology and Microbiology Department, Dasman Diabetes Institute, Dasman 15462, Kuwait.

Current issues in molecular biology
|October 28, 2025
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概括

在新陈代谢应激过程中,内质网膜 (ER) 应激会在单细胞细胞中放大血管内皮生长因子 (VEGF). 这通过活性氧物种 (ROS) 发生,将肥胖,炎症和血管生成联系起来.

关键词:
这就是ROSOS ROS.在VEGF中,VEGF是VEGF.这是一种炎症炎症炎症炎症.代谢性压力是代谢性的压力.肥胖 肥胖 肥胖 肥胖 肥胖 肥胖 肥胖 肥胖

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科学领域:

  • 生物化学 生物化学
  • 细胞生物学 细胞生物学
  • 分子生物学分子生物学

背景情况:

  • 肥胖与慢性炎症和氧化压力有关,破坏新陈代谢平衡并增加血管内皮生长因子 (VEGF).
  • 虽然缺氧和脂肪酸通过氧化应激诱导VEGF,但在单细胞中,内细胞网膜 (ER) 应激的作用尚未完全理解.

研究的目的:

  • 研究ER应激如何与代谢应激相互作用,以调节THP-1单细胞中VEGF表达的过程.
  • 阐明参与这种相互作用的机制,包括反应性氧物种 (ROS) 生产.

主要方法:

  • 使用棕酸 (PA) 的THP-1单细胞受到代谢应激,使用thapsigargin (TG) 的ER应激.
  • 测量了VEGF mRNA和蛋白质水平,ROS产生,ER压力标志物 (CHOP,ATF6,IRE1) 和抗氧化剂防御基因 (SOD2,NRF2).
  • 评估了抗氧化剂黄素对VEGF表达和ROS的影响.

主要成果:

  • 与PA和TG同时治疗与单独使用PA相比,显著增加了VEGF表达.
  • 这种增加与ROS产量增加和ER压力标志物升高有关.
  • 黄素治疗降低了VEGF表达和ROS水平,证实了ROS依赖的途径.
  • 抗氧化剂防御基因表达 (SOD2,NRF2) 被上调,表明细胞对氧化应激的反应.

结论:

  • 在脂质毒性条件下,ER压力加剧了单细胞中VEGF诱导.
  • 这种放大通过ROS介导的途径发生.
  • 这些发现表明,在与肥胖相关的疾病中,代谢压力,炎症和血管生成之间存在联系的机制.