Breaking barriers:noncanonical inflammasome executes blood–brain barrier disruption  

作　　者：Martin Dichgans Jonas J.Neher Yaw Asare 

机构地区：[1]Institute for Stroke and Dementia Research(ISD),University Hospital,Ludwig-Maximilian-University(LMU),Munich,Germany [2]Deutsches Zentrum für Neurodegenerative Erkrankungen e.V.(DZNE),Munich,Germany [3]Munich Cluster for Systems Neurology(SyNergy),Munich,Germany [4]German Center for Cardiovascular Research(DZHK),Partner Site Munich Heart Alliance(MHA),Munich,Germany [5]Biomedical Center(BMC),Biochemistry,Faculty of Medicine,LMU Munich,Munich,Germany

出　　处：《Signal Transduction and Targeted Therapy》2024年第9期3541-3543,共3页信号转导与靶向治疗（英文）

基　　金：supported by grants from the Deutsche Forschungsgemeinschaft(DFG,CRC 1123[B3],DI-722/16-1[ID:428668490],DI 722/21-1;Munich Cluster for Systems Neurology[SyNergy,EXC 2145]);a grant from the Leducq Foundation,and the Vascular Dementia Research Foundation.Y.Asare was supported by DFG(CRC 1123[B3],AS 575/1-1).

摘　　要：In a landmark study recently published in Nature,1 Wei and colleagues demonstrate that the activation of GSDMD by the cytosolic lipopolysaccharide(LPS)sensor caspase-11 triggers blood–brain barrier(BBB)breakdown upon LPS challenge independent of TLR4-induced cytokine release.Their work identifies the noncanonical inflammasome and GSDMD pore formation as a potential target for treating central nervous system(CNS)disorders associated with inflammatory BBB dysfunction.

关 键 词：inflam BARRIER CANONICAL 

分 类 号：R743.3[医药卫生—神经病学与精神病学]