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通过APE1/Ref-1氧化还原功能,可以防止VSMC通过KLF4抑制进行表型切换.

Yeon-Hee Choi1, Eunju Choi2, Sungmin Kim3

  • 1Department of Physiology, College of Medicine, Chungnam National University, Daejeon 35015, Republic of Korea.

Cellular signalling
|March 6, 2026
PubMed
概括

缺少APE1/Ref-1会增加氧化应激,促进血管光滑肌细胞 (VSMC) 切换和新极限形成. 这通过对氧化还原依赖的KLF4上调来发生,突出显示APE1/Ref-1.

关键词:
在APE1/Ref-1中使用.冠状动脉绑定 动脉绑定在KLF4KLF4氧化应激是一种氧化应激.现象型切换的切换方式血管光滑肌肉细胞细胞

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科学领域:

  • 细胞生物学 细胞生物学
  • 心血管研究研究心血管研究
  • 转毒生物学 转毒生物学

背景情况:

  • APE1/Ref-1 是一种关键蛋白质,它调节细胞的氧化还原稳定和基因表达.
  • 血管光滑肌细胞 (VSMC) 现型切换在血管疾病中至关重要.
  • 氧化应激有助于VSMC功能障碍和病态血管重塑.

研究的目的:

  • 调查APE1/Ref-1缺乏对VSMC表型切换的影响.
  • 阐明潜在的机制,包括氧化应激和KLF4.4的作用.
  • 在血管改造中评估APE1/Ref-1缺乏的体内后果.

主要方法:

  • 从异合体APE1/Ref-1缺乏的小鼠 (APE1/Ref-1+/-) 中对大动脉和VSMC进行分析.
  • 评估氧化应激标志物 (ROS,8-OHdG) 和抗氧化酶表达.
  • 对VSMC收缩和增殖标志物的评估 (SM22α,α-SMA,PCNA,KLF4).
  • 功能性研究涉及H2O2治疗,KLF4抑制/抑制和APE1/Ref-1过度表达.
  • 在APE1/Ref-1+/-小鼠的动脉绑定后的新极端形成的体内评估.

主要成果:

  • APE1/Ref-1缺乏导致VSMC的氧化应激增加和抗氧化防御降低.
  • APE1/Ref-1+/- VSMCs表现出减少的收缩标志物和增加的KLF4和PCNA表达.
  • 过氧化加剧了VSMC的表型切换,而KLF4调制逆转了这些变化.
  • APE1/Ref-1的氧化还原功能,而不是DNA修复,对于维持收缩性表型至关重要.
  • APE1/Ref-1+/-小鼠在血管损伤后表现出增加的新极度增生症.

结论:

  • APE1/Ref-1 缺乏促进VSMC表型切换和血管重塑.
  • 氧化应激介导的KLF4上调是这个过程中的关键机制.
  • APE1/Ref-1的氧化还原活性对于维持血管平衡至关重要.