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Mechanisms of TLR4-Mediated Autophagy and Nitroxidative Stress

文献类型： 外文期刊

作者： Zhang, Kunli 1 ; Huang, Qiuyan 1 ; Deng, Shoulong 3 ; Yang, Yecheng 1 ; Li, Jianhao 1 ; Wang, Sutian 1 ;

作者机构： 1.Guangdong Acad Agr Sci, Inst Anim Sci, Guangdong Key Lab Anim Breeding & Nutr, State Key Lab Livestock & Poultry Breeding, Guangzhou, Peoples R China

2.Guangdong Acad Agr Sci, Inst Anim Hlth, Guangzhou, Peoples R China

3.Chinese Acad Med Sci, Inst Lab Anim Sci, Beijing, Peoples R China

4.Peking Union Med Coll, Comparat Med Ctr, Beijing, Peoples R China

5.Foshan Univ, Guangdong Prov Key Lab Anim Mol Design & Precise, Guangdong Prov Res Ctr Gene Editing Engn Technol, Foshan, Peoples R China

关键词： TLR4; autophagy; nitroxidative stress; interaction; homeostasis

期刊名称：FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY （ 影响因子：5.293； 五年影响因子：5.882 ）

ISSN： 2235-2988

年卷期： 2021 年 11 卷

页码：

收录情况： SCI

摘要： Pathogenic infections have badly affected public health and the development of the breeding industry. Billions of dollars are spent every year fighting against these pathogens. The immune cells of a host produce reactive oxygen species and reactive nitrogen species which promote the clearance of these microbes. In addition, autophagy, which is considered an effective method to promote the destruction of pathogens, is involved in pathological processes. As research continues, the interplay between autophagy and nitroxidative stress has become apparent. Autophagy is always intertwined with nitroxidative stress. Autophagy regulates nitroxidative stress to maintain homeostasis within an appropriate range. Intracellular oxidation, in turn, is a strong inducer of autophagy. Toll-like receptor 4 (TLR4) is a pattern recognition receptor mainly involved in the regulation of inflammation during infectious diseases. Several studies have suggested that TLR4 is also a key regulator of autophagy and nitroxidative stress. In this review, we describe the role of TLR4 in autophagy and oxidation, and focus on its function in influencing autophagy-nitroxidative stress interactions.

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