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On-line Access: 2022-07-06

Received: 2021-12-08

Revision Accepted: 2022-05-03

Crosschecked: 2022-07-06

Cited: 0

Clicked: 341

Citations:  Bibtex RefMan EndNote GB/T7714


Xiaobo HU


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Journal of Zhejiang University SCIENCE B 2022 Vol.23 No.7 P.607-612


PFKL, a novel regulatory node for NOX2-dependent oxidative burst and NETosis

Author(s):  Zhaohui CAO, Di HUANG, Cifei TANG, Min ZENG, Xiaobo HU

Affiliation(s):  Department of Biochemistry and Molecular Biology, School of Basic Medicine, Hengyang Medical School, University of South China, Hengyang 421001, China; more

Corresponding email(s):   huxiaobo@foxmail.com

Key Words:  PFKL?NETosis?Neutrophil?NOX

Zhaohui CAO, Di HUANG, Cifei TANG, Min ZENG, Xiaobo HU. PFKL, a novel regulatory node for NOX2-dependent oxidative burst and NETosis[J]. Journal of Zhejiang University Science B, 2022, 23(7): 607-612.

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publisher="Zhejiang University Press & Springer",

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A1 - Zhaohui CAO
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Neutrophils are predominant leukocytes in the circulation, which are essential for killing invading pathogens via the activation of effector responses and the production of reactive oxygen species (ROS), also named as "oxidative burst." When infected, activated neutrophils fight bacteria, fungi, and viruses through oxidative burst, phagocytosis, degranulation, and the production of neutrophil extracellular traps (NETs) in a neutrophil death process named as "NETosis" (Mutua and Gershwin, 2021). NETs, consisting of DNA fibers decorated with modified histones and numerous antimicrobial proteins from cytoplasmic granules and the nucleus, can either be beneficial or detrimental (Mutua and Gershwin, 2021). Several pathways can lead to this death process. In response to various stimuli, NETosis traps and clears pathogens, facilitating phagocytosis by other neutrophils and phagocytes. However, excessive NETosis often results in disease due to increasing the pro-inflammatory response and perpetuating the inflammatory condition (Hellebrekers et al., 2018; Hidalgo et al., 2019; Klopf et al., 2021). Accordingly, inhibiting aberrant NETosis may alleviate the severity of various autoimmune and inflammatory diseases.




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