氧化应激和肺纤维化:朝着一个不利的结果路径
Patrudu Makena1, Tatiana Kikalova2, Gaddamanugu L Prasad3,4
1RAI Services Company, P.O. Box 1487, Winston-Salem, NC 27102, USA.
International journal of molecular sciences
|August 12, 2023
概括
这项研究概述了肺纤维化不良结果途径 (AOP),将肺损伤引起的氧化应激与疾病进展联系起来. 它强调香烟烟雾是关键的风险因素,为了解纤维化机制提供了一个框架.
科学领域:
- 肺部医学 肺部医学
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 肺纤维化是一种致命的,渐进的疾病,是由异常的肺上皮细胞愈合驱动的.
- 持续的肺损伤,以氧化应激和慢性炎症为特征,是纤维化发展的核心原因.
- 慢性吸烟是肺纤维化的一个重要危险因素,由于其氧化应激诱导性质.
研究的目的:
- 为研究肺纤维化机制开发一个不良结果途径 (AOP) 框架.
- 阐明吸入有毒物质 (如香烟烟雾) 造成的肺损伤导致纤维化病的途径.
- 为了提供一种机械的理解,持续的氧化压力如何导致肺纤维化.
主要方法:
- 文献审查和证据综合权重以建立AOP.
- 分子启动事件 (MIE) 的识别:氧化应激.氧化应激.
- 在该途径中定义关键事件 (KE):介质分泌,炎症细胞招募,纤维细胞激活和细胞外基质沉积.
主要成果:
- 氧化应激被认为是MIE,导致益炎和益纤维化介质的增加 (KE1).
- 这些介质触发炎性细胞招募 (KE2),其次是纤维细胞增殖和肌纤维细胞分化 (KE3).
- 增加细胞外基质沉积 (KE4) 最终导致肺纤维化.
结论:
- 开发的AOP为了解肺纤维化提供了一个机制框架.
- 它将氧化应激等分子事件与细胞和组织水平的变化联系在一起,最终导致纤维化.
- 该AOP可以帮助评估吸入的有毒物质,包括香烟烟雾在推动肺纤维化中的作用.
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