中性粒细胞胞外陷阱
细胞外
炎症
HMGB1
先天免疫系统
败血症
细胞内
免疫学
TLR4型
免疫系统
细胞生物学
医学
生物
作者
Fu-Chao Liu,Yueh-Hsun Chuang,Yung‐Fong Tsai,Huang-Ping Yu
出处
期刊:Shock
[Ovid Technologies (Wolters Kluwer)]
日期:2014-02-04
卷期号:41 (6): 491-498
被引量:65
标识
DOI:10.1097/shk.0000000000000146
摘要
Neutrophil extracellular traps (NETs), which consist of neutrophil DNA and cytoplasmic proteins, have been shown to be involved in various infectious, inflammatory, and autoimmune diseases. Neutrophil extracellular traps are abundant at the site of infection and acute inflammation. Neutrophil extracellular trap formation can occur through various intracellular signaling pathways, including peptidylarginine deiminase 4, Raf-MEK-ERK, nitric oxide, Toll-like receptor 4, high mobility group box 1, pentraxin 3, and mammalian targets of rapamycin. A growing body of evidence indicates that NETs may play an important role in injury, and decreases in NETs could reduce tissue injury. Neutrophil extracellular traps are believed to modulate the inflammatory and immune responses of individuals after injury. In this review, the role of NETs in injury, including traumatic injury, ischemia-reperfusion-induced injury, and sepsis, as well as the potential markers and therapeutic targets of NET-related injury will be discussed.
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