NLRP3炎性小体影响血管衰老的机制及其相关药物的研发

The mechanism of NLRP3 inflammasome affecting vascular aging and the development of related drugs

摘要: NOD（nucleotide binding oligomerization domain）样受体家族3（NOD-like receptor protein 3，NLRP3）炎症小体调控天冬氨酸特异蛋白酶-1（caspase-1）、白细胞介素-18（interleukin-18，IL-18）和IL-1β等细胞因子的分泌并参与衰老过程。研究发现，NLRP3炎性小体在衰老心脏和血管中被异常激活，抑制NLRP3炎性小体可缓解心脏与血管衰老。本文对NLRP3炎性小体在心脏血管衰老中的研究和相关药物进行综述，以促进NLRP3炎性小体在心血管衰老中作用机制的发现和相关药物的研发。

Abstract: Nucleotide binding oligomerization domain (NOD)-like receptor protein 3, NLRP3) inflammasomes regulate the secretion of caspase-1, interleukin-18 (IL-18), IL-1β, and other cytokines, and participates in aging. In recent years, it has been found that NLRP3 inflammasomes are abnormally activated in aging heart and vessels, and inhibition of NLRP3 inflammasomes can alleviate heart aging and vascular aging. This review summarizes the research of NLRP3 inflammasome in heart and vascular aging, and the related drugs to promote the discovery of the mechanism of NLRP3 inflammasome in heart and vascular aging and the development of related drugs.