在大动脉疾病中氧化应激诱导的DNA损伤反应途径:对炎症和血管退化的影响
Sebastian Krych1,2, Julia Gniewek2, Marek Kolbowicz3
1Department of Cardiac, Vascular and Endovascular Surgery and Transplantology, School of Medical Sciences in Zabrze, Medical University of Silesia, Marii Skłodowskiej-Curie 9, 41-800 Zabrze, Poland.
International journal of molecular sciences
|February 27, 2026
概括
氧化应激会导致大动脉细胞中的DNA损伤,激活DNA损伤反应 (DDR). 失调的DDR通过促进炎症和壁退化加速大动脉动脉瘤等大动脉疾病.
科学领域:
- 心血管生物学 心血管生物学
- 分子病理学分子病理学
- 基因组稳定性 基因组稳定性
背景情况:
- 大动脉疾病 (动脉瘤,解剖) 涉及血管壁退化和炎症.
- 氧化应激诱导的DNA损伤越来越被认为是大动脉病理的一个关键驱动因素.
- DNA损伤反应 (DDR) 网络调节了DNA损伤后的细胞命运.
研究的目的:
- 审查氧化应激,DNA损伤和大动脉病中DDR激活之间的机制联系.
- 探索DDR信号如何有助于血管重塑和大动脉壁衰弱.
- 确定大动脉疾病的潜在生物标志物和治疗点.
主要方法:
- 这部作品是对现有文学作品的叙事评论.
- 它合成了有关大动脉中氧化应激和DDR分子调节者的信息.
- 它讨论了特定基因 (OGG1,APE1,ATM,ATR,p53,PARP,NOTCH1) 和通路的作用.
主要成果:
- 氧化DNA损伤激活了血管细胞中的DDR,影响修复,亡或衰老.
- 大动脉中持续或失调的DDR信号促进慢性炎症和细胞外基质降解.
- 异常的DDR有助于血管光滑肌肉细胞表型切换,内皮功能障碍和衰老.
结论:
- DDR激活将氧化应激与主动脉的炎症和退行性途径相结合.
- 了解这些相互作用对于开发针对大动脉疾病的新疗法至关重要.
- 向DDR可能有助于保持基因组稳定性和预防大动脉事件.
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