2020
DOI: 10.1038/s41467-020-15636-8
|View full text |Cite
|
Sign up to set email alerts
|

Glycogen metabolism regulates macrophage-mediated acute inflammatory responses

Abstract: Our current understanding of how sugar metabolism affects inflammatory pathways in macrophages is incomplete. Here, we show that glycogen metabolism is an important event that controls macrophage-mediated inflammatory responses. IFN-γ/LPS treatment stimulates macrophages to synthesize glycogen, which is then channeled through glycogenolysis to generate G6P and further through the pentose phosphate pathway to yield abundant NADPH, ensuring high levels of reduced glutathione for inflammatory macrophage survival.… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
1
1
1
1

Citation Types

8
127
0

Year Published

2020
2020
2024
2024

Publication Types

Select...
9

Relationship

1
8

Authors

Journals

citations
Cited by 152 publications
(155 citation statements)
references
References 65 publications
8
127
0
Order By: Relevance
“…It remains unknown whether PBs in macrophages are consequent of endogenous glycogen metabolism and/or engulfment of exogenous PBs. Macrophages have been shown to actively metabolize glycogen, with increased synthesis and Gys1 expression regulating their inflammatory phenotype, 32 however, it remains unclear if GBE1 deficiency in this metabolic context would lead to PB formation. Speculation regarding potential macrophage engulfment of exogenous PBs is complicated by the heterogeneous roles of these cells in local and systemic immune responses 33 .…”
Section: Discussionmentioning
confidence: 99%
“…It remains unknown whether PBs in macrophages are consequent of endogenous glycogen metabolism and/or engulfment of exogenous PBs. Macrophages have been shown to actively metabolize glycogen, with increased synthesis and Gys1 expression regulating their inflammatory phenotype, 32 however, it remains unclear if GBE1 deficiency in this metabolic context would lead to PB formation. Speculation regarding potential macrophage engulfment of exogenous PBs is complicated by the heterogeneous roles of these cells in local and systemic immune responses 33 .…”
Section: Discussionmentioning
confidence: 99%
“…This observation was expanded to show that NLRP3 inflammasome priming and IL-1β secretion in dendritic cells is dependent on glycogen catabolism [104]. Interestingly, it has been shown recently that glycogen metabolism in macrophages produces an intermediate metabolite UDP-glucose, which activates STAT1-mediated inflammatory signaling transduction via the P2Y 14 receptor [105]. Whether glycogen metabolism can also activate the NLRP3 inflammasome in macrophages is still unclear.…”
Section: Glycolytic Fluxmentioning
confidence: 99%
“…Abrogation of glycogenolysis by the inhibitor PZ0189 interferes with the PPP, ultimately leading to increased ROS levels and macrophage death. Meanwhile, the disruption of glycogenolysis or PPP can inhibit the M1 phenotype and reduce macrophage ability to clear bacteria, suggesting that the glycogenolysis-directed PPP plays a critical role in regulating the phenotype, function and survival of M1 macrophages [80]. [81][82][83][84].…”
Section: Accepted Articlementioning
confidence: 99%