自噬与NLRP3炎症小体的相互作用

Interaction Between Autophagy and NLRP3 Inflammasome

自噬是一种普遍存在的细胞内稳态机制,通过将细胞质成分运送到溶酶体进行降解,以抵抗病原体感染并促进氨基酸循环。NLRP3炎症小体是一种多蛋白复合物,在多种内源和外源性刺激下被激活,介导促炎细胞因子的分泌,参与炎症的发生。自噬功能失调可导致NLRP3炎症小体的过度激活,引起各种炎症性疾病以及癌症的发生。自噬作为NLRP3炎症小体的一种重要调节方式,可以通过去除NLRP3炎症小体的激活信号、包裹和降解其成分来调控炎症小体。此外,自噬在调控IL-1β的分泌中也起着重要作用。同样,NLRP3炎症小体也调控自噬过程,以平衡宿主防御所需的适当炎症反应以及预防过度、有害炎症的发生。因此,阐明这两个生物学过程之间的相互作用,能够加深对相关疾病发病机制的认识,为疾病治疗及药物研发提供新的思路和理论基础。

Autophagy is an ubiquitous intracellular homeostatic mechanism that transports cytoplasmic components to lysosomes for degradation to resist pathogen infection and promote the circulation of amino acids.The NLR family pyrin domain containing 3(NLRP3) inflammasome is a multi-protein complex that is activated under various endogenous and exogenous stimuli. It mediates the secretion of pro-inflammatory cytokines to participate in inflammation. Dysfunction of autophagy can result in excessive activation of the NLRP3inflammasome, thereby leading to various inflammatory diseases and cancers. As an important regulator of the NLRP3 inflammasome, autophagy can remove the activation signal of the NLRP3 inflammasome, and “wrap” and degrade its components. Autophagy also plays an important part in regulation of secretion of interleukin-1β.Similarly, the NLRP3 inflammasome regulates autophagy to balance the appropriate inflammatory response and prevent excessive and harmful inflammation. Therefore, clarifying the interaction between these two biological processes can deepen understanding of the pathogenesis of related diseases, and provide new insights and theoretical foundations for disease treatment and drug development.