Mechanism of FGF2 mediated ferroptosis in renal fibrosis cells through STAT3/SLC7A11 signaling pathway
10.3969/j.issn.1000-484X.2025.05.009
- VernacularTitle:FGF2通过STAT3/SLC7A11信号通路介导肾纤维化细胞铁死亡的机制研究
- Author:
Han LI
1
;
Chaojia ZHANG
;
Hongyang DUAN
;
Weizhou YIN
;
Jinlu WU
;
Guangjian LU
Author Information
1. 南阳医学高等专科学校第一附属医院肾脏内科,南阳 473000
- Publication Type:Journal Article
- Keywords:
FGF2;
STAT3;
SLC7A11;
Renal fibrosis;
Ferroptosis
- From:
Chinese Journal of Immunology
2025;41(5):1072-1077
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To explore the effect of fibroblast growth factor 2(FGF2)on ferroptosis of renal fibrotic cells and its po-tential molecular mechanisms.Methods:Rat NRK-52E cells were randomly divided into control group,renal fibrosis model group,FGF2 cytokine stimulation group,knockdown empty plasmid group,si-FGF2 group,overexpression empty plasmid group,overexpres-sion FGF2 group,Fer-1 treatment group.The model group was treated with TGF-β1 to obtain a renal fibrosis cell model.Cellular im-munofluorescence method was used to measure the level of cell fibrosis.Western blot was used to detect ferroptosis-related proteins(Nrf2,GPX4 and SLC7A11)and pathway proteins(STAT3,p-STAT3)expression level in the cells.Results:Knockdown of FGF2 could alleviate the increase in α-SMA and Collagen Ⅲ proteins caused by TGF-β1 stimulation of renal tubular cells(P<0.05).FGF2 could promote the activation of STAT3 protein into p-STAT3.The expression level of SLC7A11 protein was significantly increased after FGF2 cytokine stimulation(P<0.05).Compared with the control group,the expressions of Nrf2 and GPX4 in renal fibrotic cells in the si-FGF2 group and Fer-1 treated group were significantly reduced(P<0.05).In addition,knockdown of FGF2 significantly reduced in-terstitial fibrosis of renal tubular epithelial cells(P<0.05).Conclusion:FGF2 may mediate TGF-β1-induced renal ferroptosis through the STAT3/SLC7A11 signaling pathway,and knock down of FGF2 can improve fibrosis of renal tubular epithelial cells.
