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TET1 减轻烟雾诱导的支气管上皮细胞亡通过Upregulating Nrf2通过缓解

Zi-Xiao Zhang¹, Hao-Da Yu¹, Xiao-Yan Sai¹

¹Department of Respiratory Medicine, The Affiliated Wuxi People's Hospital of Nanjing Medical University, Wuxi People's Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, Jiangsu, 214023, People's Republic of China.

International journal of chronic obstructive pulmonary disease

|September 19, 2025

概括

降低Nrf2表达在COPD中与促进剂高甲基化有关. TET1脱甲基还原了Nrf2,缓解了亡和氧化应激,这表明TET1是COPD的治疗点.

科学领域:

肺部医学肺部医学
表观遗传学在表观遗传学中,表观遗传学是指表观遗传学.
分子生物学分子生物学

背景情况:

核因子红色素2相关因子2 (Nrf2) 对于氧化应激反应至关重要,并且在严重的慢性阻塞性肺病 (COPD) 中降低调节.
在COPD中调节Nrf2的表观遗传机制在很大程度上是未知的.
了解这些机制对于开发新的治疗策略至关重要.

研究的目的:

研究Nrf2在COPD中的表观遗传调节.
探索十一转位甲基细胞二氧化酶1 (TET1) 在 Nrf2 调节中的作用及其对 COPD 病原性的影响.
为了确定COPD的潜在治疗点.

主要方法:

在COPD患者和对照患者的肺组织和细胞中评估了Nrf2,血氧酶-1 (HO-1),TET1和DNA甲基转移酶1 (DNMT1) 的蛋白质水平.
使用了以香烟烟雾提取物 (CSE) 处理的人类支气管上皮细胞 (HBE) 的体外模型.
通过双硫酸盐测序和TET1结合Nrf2促进体的评估Nrf2促进体甲基化使用染色体免疫沉 (ChIP).

主要成果:

在COPD患者中,Nrf2和HO-1表达显著降低.
CSE暴露增加了HBE细胞中的Nrf2促进子甲基化,而Nrf2过度表达减少了氧化应激和亡.
在COPD肺部,TET1表达减少,但TET1过度表达增强了Nrf2转录,减少了氧化损伤和亡.

结论:

在COPD中减少Nrf2表达与促进剂高甲基化有关.
TET1直接结合并去甲基化Nrf2促进体,恢复Nrf2的表达和减弱亡.
TET1代表了COPD治疗的潜在治疗标.

关键词:

通过DNA甲基化.Nrf2 没有任何问题.在TET1上.慢性阻塞性肺病慢性阻塞性肺病

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