中性粒细胞胞外陷阱
缺血
医学
冲程(发动机)
神经炎症
炎症
神经退行性变
脑缺血
创伤性脑损伤
再灌注损伤
神经科学
趋化因子
免疫学
药理学
生物信息学
疾病
内科学
生物
机械工程
精神科
工程类
作者
Haijun Luo,Hanjing Guo,Yue Zhou,Rui Fang,Wenli Zhang,Zhigang Mei
出处
期刊:Current Neuropharmacology
[Bentham Science]
日期:2023-10-01
卷期号:21 (10): 2079-2096
被引量:3
标识
DOI:10.2174/1570159x21666230308090351
摘要
Cerebral ischemic injury, one of the leading causes of morbidity and mortality worldwide, triggers various central nervous system (CNS) diseases, including acute ischemic stroke (AIS) and chronic ischemia-induced Alzheimer's disease (AD). Currently, targeted therapies are urgently needed to address neurological disorders caused by cerebral ischemia/reperfusion injury (CI/RI), and the emergence of neutrophil extracellular traps (NETs) may be able to relieve the pressure. Neutrophils are precursors to brain injury following ischemic stroke and exert complicated functions. NETs extracellularly release reticular complexes of neutrophils, i.e., double-stranded DNA (dsDNA), histones, and granulins. Paradoxically, NETs play a dual role, friend and foe, under different conditions, for example, physiological circumstances, infection, neurodegeneration, and ischemia/reperfusion. Increasing evidence indicates that NETs exert anti-inflammatory effects by degrading cytokines and chemokines through protease at a relatively stable and moderate level under physiological conditions, while excessive amounts of NETs release (NETosis) irritated by CI/RI exacerbate the inflammatory response and aggravate thrombosis, disrupt the blood-brain barrier (BBB), and initiates sequential neuron injury and tissue damage. This review provides a comprehensive overview of the machinery of NETs formation and the role of an abnormal cascade of NETs in CI/RI, as well as other ischemia-induced neurological diseases. Herein, we highlight the potential of NETs as a therapeutic target against ischemic stroke that may inspire translational research and innovative clinical approaches.
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