August 19, 2025Cell Death and DiseaseOpen Access

FGF15/FGFR4 signaling suppresses M1 macrophage polarization and multi-organ inflammation in septic mice by inhibiting H3K18 lactylation-driven Irf7 expression through NF2-Hippo activation

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FGF15 significantly suppresses M1 macrophage polarization, reducing inflammation in septic mice and enhancing survival.
The study demonstrated that rFGF15 treatment led to reduced expression of Irf7, a key regulator of interferon responses, suggesting a clear mechanism of action.
Activation of the NF2-Hippo pathway by FGF15 inhibition of H3K18 lactylation provides insight into new therapeutic strategies for sepsis treatment.
Further validation in clinical settings may enable FGF15 to serve as an innovative therapy for managing sepsis-related organ inflammation.

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Implication

Observational analysis shows FGF15 reduces M1 macrophage polarization and multi-organ inflammation in septic mice, suggesting a novel therapeutic pathway through NF2-Hippo activation.

Cite This Study

Li et al. (2025) studied this question.

synapsesocial.com/papers/68af33e9cf1dd9ea359e9248 https://doi.org/10.1038/s41419-025-07962-w

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Implication

Observational analysis shows FGF15 reduces M1 macrophage polarization and multi-organ inflammation in septic mice, suggesting a novel therapeutic pathway through NF2-Hippo activation.

FGF15/FGFR4 signaling suppresses M1 macrophage polarization and multi-organ inflammation in septic mice by inhibiting H3K18 lactylation-driven Irf7 expression through NF2-Hippo activation

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Discussion

Implication

Cite This Study

FGF15/FGFR4 signaling suppresses M1 macrophage polarization and multi-organ inflammation in septic mice by inhibiting H3K18 lactylation-driven Irf7 expression through NF2-Hippo activation

Key Points

Discussion

Implication

Cite This Study

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