FGF5 protects heart from sepsis injury by attenuating cardiomyocyte pyroptosis through inhibiting CaMKII/NFκB signaling

Cui, Shengyu; Li, Yuhua; Zhang, Xutao; Wu, Bing; Li, Ming; Gao, Jixian; Xia, Hao; Xu, Lin

doi:10.1016/j.bbrc.2022.10.080

Cited by 6 publications

(1 citation statement)

References 46 publications

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“…A total of 23 FGF molecules have been identified so far ( Ornitz & Itoh, 2001 ; Yun et al, 2010 ). A recent study found that FGF5 protects against myocardial injury caused by sepsis by inhibiting CaMKII/NF-κB signaling ( Cui et al, 2022 ). FGF2 inhibits coagulation activity in septic mice by inhibiting the AKT/mTOR/S6K1 pathway, alleviating lung and liver damage and improving survival ( Sun et al, 2023 ).…”

Section: Discussionmentioning

confidence: 99%

The causal effects of circulating cytokines on sepsis: a Mendelian randomization study

Fang,

Chai,

2024

PeerJ

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Background In observational studies, sepsis and circulating levels of cytokines have been associated with unclear causality. This study used Mendelian randomization (MR) to identify the causal direction between circulating cytokines and sepsis in a two-sample study. Methods An MR analysis was performed to estimate the causal effect of 41 cytokines on sepsis risk. The inverse-variance weighted random-effects method, the weighted median-based method, and MR-Egger were used to analyze the data. Heterogeneity and pleiotropy were assessed using MR-Egger regression and Cochran’s Q statistic. Results Genetically predicted beta-nerve growth factor (OR = 1.12, 95% CI [1.037–1.211], P = 0.004) increased the risk of sepsis, while RANTES (OR = 0.92, 95% CI [0.849–0.997], P = 0.041) and fibroblast growth factor (OR = 0.869, 95% CI [0.766–0.986], P = 0.029) reduced the risk of sepsis. These findings were robust in extensive sensitivity analyses. There was no clear association between the other cytokines and sepsis risk. Conclusion The findings of this study demonstrate that beta-nerve growth factor, RANTES, and fibroblast growth factor contribute to sepsis risk. Investigations into potential mechanisms are warranted.

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Section: Discussionmentioning

confidence: 99%

The causal effects of circulating cytokines on sepsis: a Mendelian randomization study

Fang,

Chai,

2024

PeerJ

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FGF21 ameliorates septic liver injury by restraining proinflammatory macrophages activation through the autophagy/HIF-1α axis

Zhu,

Jin,

Wang

et al. 2024

Journal of Advanced Research

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Fibroblast Growth Factor 5 Promotes the Proliferation of Corneal Epithelium Through Phosphoinositide 3-Kinase/Protein Kinase B Signaling Pathway Activation

Jiang

Zhou

et al. 2023

j biomed nanotechnol

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The recovery of corneal epithelial wounds is a complex process involving several physiological and pathological mechanisms that require further investigation. Our study has unveiled that the primary expression of FGF5 and FGFR1 occurs in the basal epithelium of the limbus. In the early 48 hours of the corneal epithelial wound healing process, FGF5 expression gradually rose and subsequently returned to baseline levels. The mice corneal epithelial cells (TKE2) proliferation was promoted by rhFGF5. Furthermore, the stemness-related genes K14, K15, P63, and the proliferation marker Ki67 levels expression increased after treatment with rhFGF5. In vivo, rhFGF5 promoted corneal epithelial wound healing. The RNA sequencing analysis of rhFGF5 treated TKE2 cells revealed 1512 differentially expressed genes. Different genes related to the cell cycle, proliferation, and regulatory signaling pathways were enriched. Moreover, the activation of the phosphoinositide 3-kinase/protein kinase B (PI3K-AKT) signaling pathway due to FGF5 led to the amplification of corneal progenitor cells. When FGF5 expression was curbed using siRNA, both proliferation and PI3K-AKT signaling pathway activation decreased. Our investigation has demonstrated that FGF5 stimulates the expansion of corneal limbal stem cells by activating the PI3K-AKT signaling pathway. Therefore, FGF5 has the potential to be an efficacious therapeutic intervention for treating corneal epithelial injuries.

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FGF5 protects heart from sepsis injury by attenuating cardiomyocyte pyroptosis through inhibiting CaMKII/NFκB signaling

Cited by 6 publications

References 46 publications

The causal effects of circulating cytokines on sepsis: a Mendelian randomization study

The causal effects of circulating cytokines on sepsis: a Mendelian randomization study

FGF21 ameliorates septic liver injury by restraining proinflammatory macrophages activation through the autophagy/HIF-1α axis

Fibroblast Growth Factor 5 Promotes the Proliferation of Corneal Epithelium Through Phosphoinositide 3-Kinase/Protein Kinase B Signaling Pathway Activation

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