摘要
创伤性脑损(traumatic brain injury, TBI)是全球脑损伤患者死亡和致残的主要原因。创伤导致的不受控的内源性介质释放作为危险信号被危险相关分子模式(damage associated molecular patterns,DAMPs)感知,触发炎性体(inflammasome)蛋白复合物组装。炎性体是TBI后的关键细胞内多蛋白信号感知平台,炎性体组装可以诱导含半胱氨酸的天冬氨酸蛋白水解酶-1(cysteinyl aspartate specific proteinase-1, caspase-1)活化促使白细胞介素(interleukin, IL)-1β和IL-18的成熟和释放,启动细胞焦亡。近年来越来越多的证据表明,炎症小体主要是NLRP3、NLRP1和AIM2介导的细胞焦亡,参与TBI后组织损伤和功能障碍。本文简要总结目前关于细胞焦亡在TBI中作用的研究进展。
Traumatic brain injury(TBI)is the leading cause of death and disability worldwide in patients with brain injury.Trauma causes uncontrolled endogenous mediator release as a danger signal to be perceived by damage-associated molecular patterns(DAMPs),triggering the assembly of intracellular multiprotein complexes named inflammasomes.The inflammasomes is a key intracellular multiprotein signaling platform after TBI.Inflammasomes assembly can induce cysteinyl aspartate specific proteinase-1(caspase-1)activation to promote the maturation and release of interleukin(IL)-1βand IL-18,and initiate pyroptosis.Accumulating data suggest that inflammasomes,mainly NLRP3,NLRP1 and AIM2,are involved in tissue damage and dysfunction following TBI.This review briefly summarizes current research advances in the role of pyroptosis in TBI.
作者
曾钧发
曾召林
慎松
任远
ZENG Junfa;ZENG Zhaolin;SHEN Song;REN Yuan(Institute of Cardiovascular Disease,Key Laboratory for Atherosclerology of Hu'nan Province,University of South China,Hengyang 421001,China;The second hospital of University of South China,Hengyang 421001,China;Department of Cardiology,People’s Hospital of Nanchuan,Chongqing Medical University,Chongqing,408499;Chongqing Jiulongpo People’s Hospital,Chongqing,400050,China)
出处
《生命的化学》
CAS
CSCD
2019年第4期736-743,共8页
Chemistry of Life
基金
南华大学研究生科学基金(2018KYY259)
