NLRP3炎性小体影响血管衰老的机制及其相关药物的研发  被引量:5

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

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作  者:吉晓漫 徐明 JI Xiao-man;XU Ming(School of Basic Medicine and Clinical Pharmacy,China Pharmaceutical University,Nanjing 211100,China)

机构地区:[1]中国药科大学基础医学与临床药学学院,江苏南京211100

出  处:《药学学报》2021年第3期696-702,共7页Acta Pharmaceutica Sinica

基  金:国家自然科学基金资助项目(81773732)。

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。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.

关 键 词:NLRP3炎性小体 心脏衰老 血管衰老 心脑血管疾病 抗衰老 senolytics 

分 类 号:R966[医药卫生—药理学]

 

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