在肺部疾病的进展中,ROS-炎症基因表达轴之间的交叉交叉
Sumel Ashique1,2, Neeraj Mishra3, Shubhrajit Mantry4
1Department of Pharmaceutics, Bengal College of Pharmaceutical Sciences & Research, Durgapur, West Bengal, 713212, India. ashiquesumel007@gmail.com.
Naunyn-Schmiedeberg's archives of pharmacology
|August 28, 2024
概括
氧化失衡导致难以治疗的炎症性肺病,因为它会导致过度反应性氧物种 (ROS) 和细胞损伤. 需要新的治疗点来对抗这种氧化应激,并改善患者的治疗结果.
科学领域:
- 肺部医学 肺部医学
- 氧化压力研究研究 氧化压力研究
- 炎症性疾病 炎症性疾病
背景情况:
- 炎症性肺部疾病导致全球显著的死亡率和残疾.
- 严重的疾病变种,如肺气,喘和COVID-19缺乏有效的治疗方法.
- 氧化失衡是发展具有挑战性的炎症性肺部疾病的关键因素.
研究的目的:
- 突出氧化失衡在严重的炎症性肺部疾病中的作用.
- 探索将反应性氧物种 (ROS) 与肺组织损伤联系起来的机制.
- 为了确定氧化应激诱导的肺炎的潜在治疗点.
主要方法:
- 关于氧化应激和炎症性肺部疾病的当前文献的综述.
- 分析涉及ROS产生和信号的途径.
- 确定治疗干预的分子点.
主要成果:
- 内源性抗氧化剂系统对诱导的ROS过度生产是不够的.
- ROS会触发促炎介质,导致组织损伤和炎症恶化.
- 增加的ROS可以导致DNA损伤,亡和原基因激活.
结论:
- 氧化应激是严重炎症性肺部疾病的关键机制.
- 准ROS途径为新的治疗策略提供了潜力.
- 对这些目标的进一步研究可能会导致对难以治疗的肺部疾病的新疗法.
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