Chongqing Key Laboratory of Neurobiology, Institute of Neuroscience, Chongqing Medical University, Chongqing 400016, China.
Department of Anatomy, Chongqing Medical University, Chongqing 400016, China.
Acta Biochim Biophys Sin (Shanghai). 2019 Nov 18;51(11):1087-1095. doi: 10.1093/abbs/gmz098.
Autophagy, a metabolic pathway that plays an important role in maintaining the dynamic balance of cells, has two types, i.e. non-selective autophagy and selective autophagy. The role of non-selective autophagy is primarily to allow cells to circulate nutrients in an energy-limited environment, while selective autophagy primarily cleans up the organelles inside the cells to maintain the cell structure. The NLRP3 inflammasome is an innate immune response produced by the organism that can promote the secretion of interleukin-1β and interleukin-18 through caspase-1 activation and resist the damage of some pathogens. However, when the NLRP3 inflammasome is overactivated, it can cause various inflammatory diseases, such as inflammatory liver disease and inflammatory bowel disease. Many previous studies have shown that autophagy can inhibit the NLRP3 inflammasome, while in recent years, new studies have found that autophagy can also promote the NLRP3 inflammasome in some cases, and the NLRP3 inflammasome can, in turn, affect autophagy. In this review, the interaction between autophagy and the NLRP3 inflammasome is explored, and then the application of this interaction in disease treatment is discussed.
自噬是一种在维持细胞动态平衡中起重要作用的代谢途径，有两种类型，即非选择性自噬和选择性自噬。非选择性自噬的作用主要是使细胞在能量有限的环境中循环利用营养物质，而选择性自噬主要是清除细胞内的细胞器，以维持细胞结构。NLRP3 炎性小体是机体产生的一种先天免疫反应，通过半胱天冬酶-1 的激活可以促进白细胞介素-1β和白细胞介素-18 的分泌，抵抗一些病原体的损害。然而，当 NLRP3 炎性小体过度激活时，会引起各种炎症性疾病，如炎症性肝病和炎症性肠病。许多先前的研究表明，自噬可以抑制 NLRP3 炎性小体，而近年来，新的研究发现，自噬在某些情况下也可以促进 NLRP3 炎性小体，而 NLRP3 炎性小体反过来又可以影响自噬。本文探讨了自噬与 NLRP3 炎性小体之间的相互作用，然后讨论了这种相互作用在疾病治疗中的应用。
