NLRP3炎症小体在动脉粥样硬化中的作用机制研究进展

Research Progress in Mechanism of NLRP3 Inflammasome in Atherosclerosis

动脉粥样硬化(As)是一种以血管炎症性为特点的疾病,是造成心脑血管疾病的主要原因之一,其具体发病机制目前尚不明确,可能与细胞自噬、内质网应激以及核因子κB(NF-κB)通路有关。核苷酸结合寡聚化结构域样受体蛋白3(NLRP3)炎症小体是参与固有免疫系统组成的蛋白体复合物。NLRP3炎症小体的激活与As的发生有紧密联系,其激活可能通过抑制细胞自噬导致活性氧堆积、诱导内质网应激发生激活未折叠蛋白反应,从而增加硫氧还蛋白互作蛋白表达并激活Toll样受体4/髓样分化因子88/NF-κB信号通路,最终引起炎症反应,促进As的发生发展。

Atherosclerosis(As)is a disease characterized by vasculitis,which is one of the main causes of cardiovascular and cerebrovascular diseases.Its specific pathogenesis is still unclear,which may be related to autophagy,endoplasmic reticulum stress and nuclear factor-κB(NF-κB)pathway.Nucleotide-binding oligomerization domain-like receptor protein 3(NLRP3)inflammasome is a protein complex involved in the composition of the innate immune system.The activation of NLRP3 inflammasome is closely related to the occurrence of As,and its activation may be achieved by inhibiting autophagy,leading to the accumulation of reactive oxygen species,inducing endoplasmic reticulum stress and activating unfolded protein responses,thereby increasing the expression of thioredoxin interacting proteins and activating Toll-like receptor 4/myeloid differentiation factor 88/NF-κB signaling pathway,which ultimately triggers an inflammatory response and promotes the occurrence and development of As.