上睑下垂
炎症体
线粒体
细胞生物学
炎症
分泌物
程序性细胞死亡
促炎细胞因子
生物
免疫学
半胱氨酸蛋白酶1
细胞凋亡
生物化学
作者
Prajwal Gurung,John R. Lukens,Thirumala‐Devi Kanneganti
标识
DOI:10.1016/j.molmed.2014.11.008
摘要
Recent studies have identified new roles for mitochondria in the regulation of autoinflammatory processes. Emerging data suggests that the release of danger signals from mitochondria in response to stress and infection promotes the formation of the inflammatory signaling platform known as inflammasomes. Activation of inflammasomes by damaged mitochondria results in caspase-1-dependent secretion of the inflammatory cytokines interleukin-1β (IL-1β) and IL-18, and an inflammatory form of cell death referred to as pyroptosis. Here, we review recently described mechanisms that have been proposed to be involved in mitochondria-mediated regulation of inflammasome activation and inflammation. In addition, we highlight how aberrant regulation of mitochondria-induced inflammasome activation centrally contributes to the inflammatory process that is responsible for obesity and associated metabolic diseases.
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