Numan Mohamed Saber, Brown Jacques P, Michou Laëtitia
Department of Endocrinology and Nephrology, Centre Hospitalier Universitaire de Québec Research Centre, Québec, QC, G1V 4G2, Canada.
Division of Rheumatology, Department of Medicine, University Laval, Québec, QC, G1V 4G2, Canada.
Int J Environ Res Public Health. 2015 Feb 17;12(2):2289-305. doi: 10.3390/ijerph120202289.
Atmospheric pollution-induced cellular oxidative stress is probably one of the pathogenic mechanisms involved in most of the common autophagy-mediated aging diseases, including neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), Alzheimer's, disease, as well as Paget's disease of bone with or without frontotemporal dementia and inclusion body myopathy. Oxidative stress has serious damaging effects on the cellular contents: DNA, RNA, cellular proteins, and cellular organelles. Autophagy has a pivotal role in recycling these damaged non-functional organelles and misfolded or unfolded proteins. In this paper, we highlight, through a narrative review of the literature, that when autophagy processes are impaired during aging, in presence of cumulative air pollution-induced cellular oxidative stress and due to a direct effect on air pollutant, autophagy-mediated aging diseases may occur.
大气污染诱导的细胞氧化应激可能是大多数常见的自噬介导的衰老相关疾病的致病机制之一,这些疾病包括神经退行性疾病,如肌萎缩侧索硬化症(ALS)、阿尔茨海默病,以及伴有或不伴有额颞叶痴呆和包涵体肌病的佩吉特骨病。氧化应激对细胞成分(DNA、RNA、细胞蛋白和细胞器)具有严重的破坏作用。自噬在回收这些受损的无功能细胞器以及错误折叠或未折叠的蛋白质方面起着关键作用。在本文中,我们通过对文献的叙述性综述强调,在衰老过程中,当自噬过程受损时,在累积的空气污染诱导的细胞氧化应激存在的情况下,并且由于空气污染物的直接作用,可能会发生自噬介导的衰老相关疾病。