Role of neutrophil extracellular traps following injury
Journal
Shock
Journal Volume
41
Journal Issue
6
Pages
491-498
Date Issued
2014
Author(s)
Abstract
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. Copyright ? 2014 by the Shock Society.
Subjects
injury; Neutrophil extracellular trap
SDGs
Other Subjects
deoxyribonuclease; high mobility group B1 protein; histone; mammalian target of rapamycin; mek protein; membrane protein; mitogen activated protein kinase; nitric oxide; pentraxin 3; peptidylarginine deiminase 4; protein arginine deiminase; Raf protein; reduced nicotinamide adenine dinucleotide phosphate oxidase; unclassified drug; human; neutrophil; neutrophil extracellular trap; nonhuman; organ injury; reperfusion injury; review; sepsis; signal transduction; thrombocyte; tissue injury; animal; extracellular trap; injury; pathophysiology; physiology; Animals; Extracellular Traps; Humans; Signal Transduction; Wounds and Injuries
Type
journal article