ArticleNature communications2026
FGF 13 functions as a regulator of the ERK/aerobic glycolysis axis in the inflammatory state during septic lung injury.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Macrophage metabolic reprogramming in sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2026Review
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Authors and funding
17 authors.
Funding
Abstract
Fibroblast growth factor 13 (FGF13) belongs to the FGF homologous factor subfamily, members of which lack signal peptides. In this study, we demonstrate that FGF13 is significantly downregulated in endothelial cells and macrophages in the lungs of septic patients and septic mice. However, the role of FGF13 in sepsis and the underlying mechanism are largely unknown. By using mice with conditional Fgf13 knockout and FGF13 overexpression, we find that FGF13 accelerates septic lung injury by promoting inflammatory activation of endothelial cells and macrophages. Specifically, FGF13 functions as a scaffold protein in TAK1/MEK/ERK signaling to promote hypoxia-inducible factor (HIF)-1α-regulated aerobic glycolysis in the inflammatory state. Meanwhile, the protective effect of conditional Fgf13 knockout is abolished in HIF-1α-overexpressing mice. In addition, SCH772984 (a selective antagonist of ERK signaling) abolishes the aggravation of inflammation in lungs induced by FGF13 overexpression. Our findings demonstrate that FGF13 promotes inflammatory activation upon septic lung injury through the ERK/aerobic glycolysis axis, thereby accelerating the progression of septic lung injury.
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