通过抑制线粒体功能障碍和炎症,NOX4是感染性急性损伤的潜在治疗标
Jiameng Li1, Liya Wang2, Bo Wang2
1Center of Gerontology and Geriatrics, West China Hospital, Sichuan University, Chengdu 610041, China.
Theranostics
|June 7, 2023
概括
尼古丁胺胺氨基二核酸 (NADPH) 氧化酶4 (NOX4) 抑制可以防止败血性急性损伤 (S-AKI). 向NOX4可以减少活性氧物种 (ROS) 和NF-κB信号传递,减轻脏损伤.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 分子生物学分子生物学
- 病理生理学 病理生理学
背景情况:
- 败血症引起的急性损伤 (S-AKI) 是致病率和死亡率的主要原因.
- 在S-AKI中尼古丁胺胺氨基二核酸 (NADPH) 氧化酶4 (NOX4) 的作用尚不清楚.
- NOX4与各种脏疾病有关.
研究的目的:
- 调查NOX4在败血性急性损伤 (S-AKI) 中的作用和调节.
- 探索NOX4作为S-AKI的潜在治疗点.
主要方法:
- 在体内模型:使用脂聚糖化物 (LPS) 或结和穿孔 (CLP) 的野生类型和NOX4敲击小鼠的败血症诱导的急性损伤 (S-AKI).
- 试验室模型:用LPS治疗的小鼠脏管状上皮细胞 (TCMK-1).
- 评估生化,线粒体,炎症和亡参数,以及活性氧物种 (ROS) 和NF-κB信号.
主要成果:
- 在S-AKI期间,管状上皮细胞 (RTEC) 中NOX4的上调.
- 在S-AKI模型中,NOX4的遗传或药理抑制改善了功能障碍和病理.
- NOX4抑制减少了线粒体功能障碍,炎症和亡,而过度表达加剧了这些影响.
结论:
- 对NOX4的遗传或药理抑制可以防止S-AKI.
- 通过减少ROS生成和NF-κB信号激活,NOX4抑制可以减轻S-AKI.
- NOX4是S-AKI的一个有前途的治疗点.
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