Publication:
Role of neutrophil extracellular traps following injury

cris.lastimport.scopus2025-05-08T21:43:32Z
cris.virtual.departmentAnesthesiology-NTUH
cris.virtual.departmentAnesthesiology
cris.virtual.orcid0000-0003-2032-7396
cris.virtualsource.department92ea36ef-0858-4ed5-8e1b-44595ec4902e
cris.virtualsource.department92ea36ef-0858-4ed5-8e1b-44595ec4902e
cris.virtualsource.orcid92ea36ef-0858-4ed5-8e1b-44595ec4902e
dc.contributor.authorLiu, Fu-Chaoen_US
dc.contributor.authorYUEH-HSUN CHUANGen_US
dc.contributor.authorTsai, Yung-Fongen_US
dc.contributor.authorYu, Huang-Pingen_US
dc.creatorLiu, F.-C. and Chuang, Y.-H. and Tsai, Y.-F. and Yu, H.-P.
dc.date.accessioned2018-09-10T14:51:12Z
dc.date.available2018-09-10T14:51:12Z
dc.date.issued2014
dc.description.abstractNeutrophil 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.en_US
dc.identifier.doi10.1097/SHK.0000000000000146
dc.identifier.urihttp://www.scopus.com/inward/record.url?eid=2-s2.0-84901405851&partnerID=MN8TOARS
dc.identifier.urihttp://scholars.lib.ntu.edu.tw/handle/123456789/383648
dc.languageenen
dc.relation.ispartofShocken_US
dc.relation.journalissue6en_US
dc.relation.journalvolume41en_US
dc.relation.pages491-498en_US
dc.sourceAH
dc.subjectinjury; Neutrophil extracellular trapen_US
dc.subject.classification[SDGs]SDG3
dc.subject.otherdeoxyribonuclease; 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
dc.titleRole of neutrophil extracellular traps following injuryen_US
dc.typejournal articleen
dspace.entity.typePublication

Files