期刊
THESCIENTIFICWORLDJOURNAL
卷 10, 期 -, 页码 1731-1748出版社
HINDAWI LTD
DOI: 10.1100/tsw.2010.169
关键词
neutrophils; apoptosis; programmed cell death; inflammation; resolution of inflammation; anti-inflammatory; mediators; intracellular signaling; lipoxins; cyclin-dependent kinase inhibitors; PDE4 inhibitors; NF-kappa B inhibitors; beta(2) integrin; formyl peptide receptors; airway inflammation; acute lung injury; sepsis; arthritis; ischemia/reperfusion; bacterial meningitis; trauma
资金
- Canadian Institutes of Health Research [MOP-64283, MOP-67054]
Neutrophil granulocytes play a central role in host defense to infection and tissue injury. Their timely removal is essential for resolution of inflammation. Increasing evidence identified neutrophil apoptosis as an important control point in the development and resolution of inflammation. Delayed apoptosis and/or impaired clearance of neutrophils aggravate and prolong tissue injury. This review will focus on outside-in signals that provide survival cues for neutrophils, the hierarchy of pro-and antiapoptotic signals, and molecular targets in the antiapoptotic signaling network that can be exploited by endogenously produced bioactive lipids, such as lipoxins or pharmacological inhibitors, including cyclin-dependent kinase inhibitors, to redirect neutrophils to apoptosis in vivo, thus promoting resolution of inflammation.
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