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抗氧化剂和azd0156在自性受损巨细胞中拯救炎症反应

Abdalla Elbialy¹, Mai Kitauchi¹, Dai Yamanouchi¹

¹Division of Vascular Surgery, Department of Surgery, University of Wisconsin School of Medicine and Public Health, 1111 Highland Avenue, WIMR 5151, Madison, WI 53705, USA.

International journal of molecular sciences

|January 11, 2024

概括

自性缺陷通过一种新的途径驱动巨细胞炎症,包括DNA损伤和ATM激活. 针对这种自-ATM轴,为炎症性疾病提供了新的治疗策略.

科学领域:

细胞生物学细胞生物学
免疫学免疫学免疫学
分子医学是分子医学.

背景情况:

自是一种关键的细胞过程,用于降解受损的组件.
炎症性巨细胞与诸如动脉样硬化等与年龄相关的疾病有关.
以前的研究将自与巨细胞炎症联系在一起,但存在其他途径.

研究的目的:

为了研究自在巨细胞炎症中的作用.
为了确定驱动自缺陷巨细胞中炎症的新机制.
探索炎症性疾病的治疗点.

主要方法:

在THP1巨中抑制自.
用抗氧化剂和ATM抑制剂进行治疗 (azd0156).
分析M1和M2巨细胞两极分化和相关的自/DNA损伤.

主要成果:

自抑制增加了炎症基因表达 (p65介导).
这种效应被抗氧化剂或ATM抑制逆转.
M1巨细胞显示抑制自和诱导DNA损伤;M2巨细胞显示相反.
在M1/M2极化期间调节自或ATM影响了他们的炎症表型.

结论:

一个新的自-ATM通路驱动巨细胞炎症.
针对这种途径可以调节M1/M2巨细胞表型和炎症.
这一途径代表了潜在的炎症条件的治疗点.

关键词:

在 NF-kBB 中.腹部大动脉动脉瘤腹部大动脉动脉瘤亚达克西亚 telangiectasia 突变的突变的自自是自的过程.巨细胞是一个巨细胞.

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