Open AccessApelin-13 Attenuates Lipopolysaccharide-Induced Inflammatory Responses and Acute Lung Injury by Regulating PFKFB3-Driven Glycolysis Induced by NOX4-Dependent ROS
Author(s) -
Yafei Yuan,
Wei Wang,
Yue Zhang,
Qiaohui Hong,
Wenhui Huang,
Lijuan Li,
Zhanzhan Xie,
Yixin Chen,
Li Xu,
Ying Meng
Publication year - 2022
Publication title -
journal of inflammation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.656
H-Index - 33
ISSN - 1178-7031
DOI - 10.2147/jir.s348850
Subject(s) - nox4 , lipopolysaccharide , glycolysis , inflammation , proinflammatory cytokine , chemistry , medicine , pharmacology , reactive oxygen species , immunology , nadph oxidase , enzyme , biochemistry
Acute lung injury (ALI) is a life-threatening condition with limited therapeutic options. Macrophage inflammation plays a key role in the development of ALI. Abnormal glycolysis of macrophages contributes to the inflammatory response. However, the role of macrophage glycolysis in ALI still requires investigation. Apelin-13 has been shown to protect against ALI, whereas the underlying mechanisms remain unclear. In this study, we explored the effect of apelin-13 on lipopolysaccharide (LPS)-induced inflammation and ALI via regulation of glycolysis by modulating redox homeostasis in macrophages.