空气污染加剧了缺血-再输血诱导的急性损伤
Talita Rojas Sanches1, Antonio Carlos Parra1, Peiqi Sun2
1Laboratory of Basic Science in Renal Diseases (LIM-12), Division of Nephrology, School of Medicine, University of São Paulo, São Paulo, Brazil.
The Journal of pathology
|June 27, 2024
概括
暴露于细颗粒物 (PM2.5) 会使急性损伤 (AKI) 从缺血-再输液损伤 (IRI) 恶化. 暴露于PM2.5会增加AKI患者患慢性病 (CKD) 的易感性.
科学领域:
- 环境健康 环境健康
- 腎臟病學 (nephrology) 是一種醫學專業.
- 毒理学 毒理学 毒理学
背景情况:
- 慢性病 (CKD) 是一个日益严重的全球健康问题.
- 细颗粒物 (PM2.5) 暴露与功能下降有关.
- 缺血-再输液损伤 (IRI) 诱导的急性损伤 (AKI) 与PM2.5毒性共享机制,是CKD风险因素.
研究的目的:
- 调查PM2.5暴露对IRI诱导的AKI的影响.
- 探索PM2.5对损伤的影响背后的细胞和分子机制.
主要方法:
- 在接受IRI之前,小鼠被暴露在PM2.5或过空气中12周.
- 评估了功能,管状损伤,免疫反应,线粒体功能和cGAS-STING通路.
- 在体外研究中使用了暴露于PM2.5和低氧/低氧化的近接管状上皮细胞.
主要成果:
- 暴露于PM2.5加剧了IRI诱导的AKI,导致淋巴膜过率降低和尿度受损.
- PM2.5加剧了炎症,线粒体功能障碍和cGAS-STING通路的激活,导致衰老和纤维化.
- 在体外,PM2.5和低氧/低氧化增加了STING激活和管道损伤.
结论:
- PM2.5使细胞对IRI敏感,增加了对AKI的敏感性.
- 暴露于PM2.5可能会增加从AKI发展为CKD的风险.
- 减少PM2.5暴露可以改善AKI患者的治疗结果,并预防CKD的发展.
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