期刊
BIOCHEMICAL SOCIETY TRANSACTIONS
卷 35, 期 -, 页码 288-291出版社
PORTLAND PRESS LTD
DOI: 10.1042/BST0350288
关键词
apoptosis; eosinophil; inflammation; neutrophil; resolution of inflammatory response
资金
- Medical Research Council [G0601481] Funding Source: researchfish
- MRC [G0601481] Funding Source: UKRI
- Medical Research Council [G0601481] Funding Source: Medline
Apoptosis of granulocytes and the subsequent clearance of apoptotic cells are important processes for the successful resolution of inflammation. Signalling pathways, including those involving NF-kappa B (nuclear factor ice), MAPK (mitogen-activated protein kinase) and PI3K (phosphoinositide 3-kinase) have been shown to be key regulators of inflammatory cell, survival and apoptosis in vitro. In addition, manipulation of such pathways in vivo has indicated that they also play a role in the resolution of inflammation. Furthermore, manipulation of proteins directly involved in the control of apoptosis, such as Bcl-2 family members and caspases, can be targeted in vivo to influence inflammatory resolution. Recently, it has been shown that CDK (cyclin-dependent kinase) inhibitor drugs induce caspase-dependent human neutrophil apoptosis possibly by altering levels of the anti-apoptotic 8c1-2 family member, Mcl-1. Importantly, CDK inhibitor drugs augment the resolution of established 'neutrophil-dominant' inflammation by promoting apoptosis of neutrophils. Thus manipulation of apoptotic pathways, together with ensuring macrophage clearance of apoptotic cells, appears to be a viable pharmacological target for reducing established inflammation.
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