Henan International Joint Laboratory of Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng 475000, China.
Int J Mol Sci. 2021 Aug 16;22(16):8773. doi: 10.3390/ijms22168773.
Ischemia/reperfusion (I/R) injury is characterized by a limited blood supply to organs, followed by the restoration of blood flow and reoxygenation. In addition to ischemia, blood flow recovery can also lead to very harmful injury, especially inflammatory injury. Autophagy refers to the transport of cellular materials to the lysosomes for degradation, leading to the conversion of cellular components and offering energy and macromolecular precursors. It can maintain the balance of synthesis, decomposition and reuse of the intracellular components, and participate in many physiological processes and diseases. Inflammasomes are a kind of protein complex. Under physiological and pathological conditions, as the cellular innate immune signal receptors, inflammasomes sense pathogens to trigger an inflammatory response. TheNLRP3 inflammasome is the most deeply studied inflammasome and is composed of NLRP3, the adaptor apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) and pro-caspase-1. Its activation triggers the cleavage of pro-interleukin (IL)-1β and pro-IL-18 mediated by caspase-1 and promotes a further inflammatory process. Studies have shown that autophagy and the NLRP3 inflammasome play an important role in the process of I/R injury, but the relevant mechanisms have not been fully explained, especially how the interaction between autophagy and the NLRP3 inflammasome participates in I/R injury, which remains to be further studied. Therefore, we reviewed the recent studies about the interplay between autophagy and the NLRP3 inflammasome in I/R injury and analyzed the mechanisms to provide the theoretical references for further research in the future.
缺血再灌注（I/R）损伤的特征是器官的血液供应有限，随后恢复血流和再氧合。除了缺血外，血流恢复也可能导致非常有害的损伤，特别是炎症损伤。自噬是指细胞物质被运送到溶酶体进行降解，导致细胞成分的转化，并提供能量和大分子前体。它可以维持细胞内成分的合成、分解和再利用的平衡，并参与许多生理过程和疾病。炎症小体是一种蛋白质复合物。在生理和病理条件下，作为细胞先天免疫信号受体，炎症小体感知病原体触发炎症反应。NLRP3 炎症小体是研究最深入的炎症小体，由 NLRP3、衔接子凋亡相关斑点样蛋白包含一个半胱氨酸蛋白酶募集结构域（ASC）和前胱天蛋白酶-1组成。其激活触发半胱天冬酶-1介导的前白细胞介素（IL）-1β和前白细胞介素-18的切割，并促进进一步的炎症过程。研究表明，自噬和 NLRP3 炎症小体在 I/R 损伤过程中发挥重要作用，但相关机制尚未完全阐明，特别是自噬和 NLRP3 炎症小体之间的相互作用如何参与 I/R 损伤，这仍有待进一步研究。因此，我们综述了自噬与 NLRP3 炎症小体在 I/R 损伤中的相互作用的最新研究，并分析了相关机制，为未来的进一步研究提供理论参考。
