免疫球蛋白轻链
浆细胞失调
淀粉样变性
淀粉样蛋白(真菌学)
淀粉样变性
化学
分泌物
细胞生物学
生物
生物化学
免疫学
医学
病理
抗体
无机化学
作者
Chunlan Zhang,Xiao Ping Huang,Jian Li
出处
期刊:Blood Reviews
[Elsevier BV]
日期:2017-07-01
卷期号:31 (4): 261-270
被引量:18
标识
DOI:10.1016/j.blre.2017.03.002
摘要
Amyloid light-chain (AL) amyloidosis is a plasma-cell dyscrasia, as well as the most common type of systematic amyloidosis. Pathogenic plasma cells that have distinct cytogenetic and molecular properties secrete an excess amount of amyloidogenic light chains. Assisted by post-translational modifications, matrix components, and other environmental factors, these light chains undergo a conformational change that triggers the formation of amyloid fibrils that overrides the extracellular protein quality control system. Moreover, the amyloidogenic light-chain itself is cytotoxic. As a consequence, organ dysfunction is caused by both organ architecture disruption and the direct cytotoxic effect of amyloidogenic light chains. Here, we reviewed the molecular mechanisms underlying this sequence of events that ultimately leads to AL amyloidosis and also discuss current in vitro and in vivo models, as well as relevant novel therapeutic approaches.
科研通智能强力驱动
Strongly Powered by AbleSci AI