Zhao Shizhen, Li Xiaotian, Wang Jie, Wang Honggang
Henan International Joint Laboratory of Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng, China.
Front Cell Dev Biol. 2021 May 17;9:657478. doi: 10.3389/fcell.2021.657478. eCollection 2021.
Autophagy is a stable self-sustaining process in eukaryotic cells. In this process, pathogens, abnormal proteins, and organelles are encapsulated by a bilayer membrane to form autophagosomes, which are then transferred to lysosomes for degradation. Autophagy is involved in many physiological and pathological processes. Nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome, containing NLRP3, apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and pro-caspase-1, can activate caspase-1 to induce pyroptosis and lead to the maturation and secretion of interleukin-1 β (IL-1 β) and IL-18. NLRP3 inflammasome is related to many diseases. In recent years, autophagy has been reported to play a vital role by regulating the NLRP3 inflammasome in inflammatory nervous system diseases. However, the related mechanisms are not completely clarified. In this review, we sum up recent research about the role of the effects of autophagy on NLRP3 inflammasome in Alzheimer's disease, chronic cerebral hypoperfusion, Parkinson's disease, depression, cerebral ischemia/reperfusion injury, early brain injury after subarachnoid hemorrhage, and experimental autoimmune encephalomyelitis and analyzed the related mechanism to provide theoretical reference for the future research of inflammatory neurological diseases.
自噬是真核细胞中一个稳定的自我维持过程。在此过程中，病原体、异常蛋白质和细胞器被双层膜包裹形成自噬体，然后自噬体被转运至溶酶体进行降解。自噬参与许多生理和病理过程。核苷酸结合寡聚化结构域样受体蛋白3（NLRP3）炎性小体包含NLRP3、含半胱天冬酶募集结构域的凋亡相关斑点样蛋白（ASC）和前半胱天冬酶-1，可激活半胱天冬酶-1以诱导细胞焦亡，并导致白细胞介素-1β（IL-1β）和IL-18的成熟与分泌。NLRP3炎性小体与许多疾病相关。近年来，有报道称自噬在炎性神经系统疾病中通过调节NLRP3炎性小体发挥重要作用。然而，相关机制尚未完全阐明。在本综述中，我们总结了近期关于自噬对阿尔茨海默病、慢性脑灌注不足、帕金森病、抑郁症、脑缺血/再灌注损伤、蛛网膜下腔出血后早期脑损伤及实验性自身免疫性脑脊髓炎中NLRP3炎性小体影响作用的研究，并分析了相关机制，为炎性神经疾病的未来研究提供理论参考。
