The NLRP3 inflammasome has recently emerged as an unexpected marker of stress and metabolic risk and has also been implicated in the development of major aging-related diseases such as gout, type 2 diabetes, obesity, cancer, and neurodegenerative and cardiovascular disorders. Several pathways regulating the NLRP3 inflammasome are currently being studied, but how the NLRP3 inflammasome is regulated remains unknown. AMP-activated protein kinase (AMPK), a central regulator of multiple metabolic pathways involved in the pathophysiology of aging and age-related diseases, has emerged as an important integrator of signals controlling inflammation including the inflammasome. In this Opinion article, we show that several AMPK-dependent pathways regulate NLRP3 inflammasome activation during aging, suggesting NLRP3 as a potential pharmacological target in age-related diseases.

中文翻译：

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NLRP3 炎症小体在衰老过程中的 AMP 活化蛋白激酶调节

NLRP3 炎症小体最近已成为压力和代谢风险的意外标志，并且还与主要衰老相关疾病的发生有关，例如痛风、2 型糖尿病、肥胖症、癌症以及神经退行性疾病和心血管疾病。目前正在研究调节 NLRP3 炎症小体的几种途径，但如何调节 NLRP3 炎症小体仍然未知。AMP 活化蛋白激酶 (AMPK) 是参与衰老和年龄相关疾病病理生理学的多种代谢途径的中央调节剂，已成为控制炎症（包括炎症小体）信号的重要整合者。在这篇意见文章中，我们展示了几种 AMPK 依赖性通路在衰老过程中调节 NLRP3 炎症小体的激活，