PM2.5污染与内质网应激反应

Eric Heng, Areeba Maysun, Kezhong Zhang
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引用次数: 0

摘要

空气污染是城市地区一般人口的一个持续的公共健康问题,特别是对那些生活在交通密集或工业活动地区的人。越来越多的证据证实,空气动力学直径<2.5 μm (PM2.5)的环境细颗粒物暴露与心血管和代谢性疾病相关的发病率和死亡率增加之间存在显著关联。已经确定炎症和细胞内应激反应在pm2.5引起的发病机制中起重要作用。未折叠蛋白反应(UPR)是一种来自内质网(ER)的细胞内应激信号,帮助细胞从未折叠或错误折叠蛋白积累引起的应激中恢复过来。暴露于高水平的与环境相关的PM2.5可能直接或间接地中断内质网中的蛋白质折叠过程,导致内质网应激。许多研究表明,在PM2.5暴露下,内质网应激反应(UPR)与线粒体应激和炎症反应相互作用,以调节参与心血管、代谢和神经退行性疾病发展的特殊细胞类型的功能和存活。在这篇综述中,我们总结了PM2.5与内质网应激反应之间机制联系的最新进展。
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PM2.5 pollution and endoplasmic reticulum stress response
Air pollution is a sustained problem of public health for the general population in urban areas, especially for those living in areas of intensive traffic or industrial activity. Accumulating evidence has confirmed a significant association between exposure to fine ambient particulate matter with aerodynamic diameters <2.5 μm (PM2.5) and the increase of morbidity and mortality associated with cardiovascular and metabolic diseases. It has been identified that inflammation and intracellular stress responses play important roles in PM2.5-caused pathogenesis. Unfolded protein response (UPR) is an intracellular stress signaling from the endoplasmic reticulum (ER) to help cell recovery from the stress caused by the accumulation of unfolded or misfolded proteins. Exposure to high levels of environmentally relevant PM2.5 may directly or indirectly interrupt the protein folding process in the ER, causing ER stress. A number of studies suggested that ER stress response, or UPR, interacts with mitochondrial stress and inflammatory responses, under PM2.5 exposure, to modulate functions and survival of specialized cell types that are involved in the development of cardiovascular, metabolic, and neurodegenerative diseases. In this review, we summarize the recent advance in understanding the mechanistic links between PM2.5 and ER stress response.
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