Mitochondrial reactive oxygen species drive proinflammatory cytokine production

被引：588

作者：

Naik, Edwina ^{[1
]}

Dixit, Vishva M. ^{[1
]}

机构：

[1] Genentech Inc, San Francisco, CA 94080 USA

来源：

JOURNAL OF EXPERIMENTAL MEDICINE | 2011年 / 208卷 / 03期

关键词：

TNF RECEPTOR; ACTIVATION; DISEASE;

D O I：

10.1084/jem.20110367

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

High levels of reactive oxygen species (ROS) are observed in chronic human diseases such as neurodegeneration, Crohn's disease, and cancer. In addition to the presence of oxidative stress, these diseases are also characterized by deregulated inflammatory responses, including but not limited to proinflammatory cytokine production. New work exploring the mechanisms linking ROS and inflammation find that ROS derived from mitochondria act as signal-transducing molecules that provoke the up-regulation of inflammatory cytokine subsets via distinct molecular pathways.

引用

页码：417 / 420

页数：4

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