Department of Clinical Pharmacy, the First Hospital of Jilin University, Changchun, , Jilin, China.
School of Pharmaceutical Science, Jilin University, Changchun, Jilin, China.
Cell Commun Signal. 2023 Jul 28;21(1):185. doi: 10.1186/s12964-023-01177-2.
The silent information regulator 2 homolog 1-NACHT, LRR and PYD domains-containing protein 3 (SIRT1-NLRP3) pathway has a crucial role in regulation of the inflammatory response, and is closely related to the occurrence and development of several inflammation-related diseases. NLRP3 is activated to produce the NLRP3 inflammasome, which leads to activation of caspase-1 and cleavage of pro-interleukin (IL)-1β and pro-IL-18 to their active forms: IL-1β and IL-18, respectively. They are proinflammatory cytokines which then cause an inflammatory response.SIRT1 can inhibit this inflammatory response through nuclear factor erythroid 2-related factor 2 and nuclear factor-kappa B pathways. This review article focuses mainly on how the SIRT1-NLRP3 pathway influences the inflammatory response and its relationship with melatonin, traumatic brain injury, neuroinflammation, depression, atherosclerosis, and liver damage. Video Abstract.
沉默信息调节因子 2 同源物 1-NACHT、LRR 和 PYD 结构域包含蛋白 3（SIRT1-NLRP3）途径在调节炎症反应中具有关键作用，并且与几种炎症相关疾病的发生和发展密切相关。NLRP3 被激活以产生 NLRP3 炎性小体，导致半胱天冬酶-1 的激活和前白细胞介素 (IL)-1β 和前白细胞介素 (IL)-18 的切割为其活性形式：IL-1β 和 IL-18，分别。它们是促炎细胞因子，然后引起炎症反应。SIRT1 可以通过核因子红细胞 2 相关因子 2 和核因子-κB 途径抑制这种炎症反应。本文主要综述了 SIRT1-NLRP3 途径如何影响炎症反应及其与褪黑素、创伤性脑损伤、神经炎症、抑郁、动脉粥样硬化和肝损伤的关系。视频摘要。
