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ROS-activated CXCR2+ neutrophils recruited by CXCL1 delay denervated skeletal muscle atrophy and undergo P53-mediated apoptosis

Medicine and Health

ROS-activated CXCR2+ neutrophils recruited by CXCL1 delay denervated skeletal muscle atrophy and undergo P53-mediated apoptosis

Y. Xiang, J. Dai, et al.

Discover how reactive oxygen species (ROS) activate neutrophils to combat muscle atrophy following denervation in this groundbreaking research by Yaoxian Xiang and colleagues. Their study reveals a potential therapeutic target in neutrophils for treating skeletal muscle atrophy, presenting exciting new avenues for intervention.

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Playback language: English
Abstract
This study investigated the role of neutrophils in denervated skeletal muscle atrophy. Using intravital imaging, flow cytometry, and transcriptome analysis, the researchers demonstrated that reactive oxygen species (ROS) activate neutrophils after denervation, leading to their recruitment to the muscle tissue via CXCL1-mediated chemotaxis. These CXCR2+ neutrophils delay atrophy before undergoing P53-mediated apoptosis within a week. The findings suggest neutrophils are a potential therapeutic target for denervated muscle atrophy.
Publisher
Experimental & Molecular Medicine
Published On
Jul 21, 2022
Authors
Yaoxian Xiang, Junxi Dai, Yao Li, Zongqi You, Junpeng Zhang, Xinying Huang, Shuqi Nie, Yujie Chen, Lei Xu, Fengming Liu, Junjian Jiang, Jianguang Xu
Tags
neutrophils
muscle atrophy
denervation
reactive oxygen species
chemotaxis
CXCL1
therapeutic target

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