Basic & Clinical Medicine ›› 2025, Vol. 45 ›› Issue (12): 1541-1547.doi: 10.16352/j.issn.1001-6325.2025.12.1541

• Original Articles • Previous Articles     Next Articles

Decreased expression of SFXNs in renal tissues of mouse models of acute and chronic kidney disease

GAO Li1,2#, WANG Siyi2,3#, ZHANG Minjing2, ZHAO Lin2, XU Zheming2, ZHANG Gensheng2, YAN Jieping1*   

  1. 1. Department of Pharmacy, Center for Clinical Pharmacy, Zhejiang Provincial People′s Hospital, People′s Hospital Affiliated to Hangzhou Medical College, Hangzhou 310014;
    2. Children′s Hospital, Zhejiang University School of Medicine, National Clinical Research Center for Child Health, Hangzhou 310052;
    3. Department of Pharmacology, College of Pharmaceutical Sciences, Zhejiang University of Technology, Hangzhou 310014, China
  • Received:2024-11-22 Revised:2025-02-26 Online:2025-12-05 Published:2025-11-25
  • Contact: *yanjieping@hmc.edu.cn

Abstract: Objective To investigate the expression changes of iron autophagy-mitochondrial ferric ion transport protein families (SFXNs) in acute kidney injury (AKI) and chronic kidney disease (CKD) mouse models induced by cisplatin (Cis) and ischemia reperfusion (IR). Methods C57BL/6 mice were randomly divided into control group (control), Cis-AKI group, Cis-CKD group, sham-operated group (sham), IR-AKI group, and IR-CKD group. Serum and kidney tissue samples were collected from mice. Serum creatinine (Cr) and blood urea nitrogen (BUN) levels were detected. Pathological changes in renal tissues were observed by HE staining. Western blot was used to detect the expression of renal SFXNs and kidney injury related proteins. Results Compared with the control or sham group, the levels of BUN and Cr in the serum of the model group were significantly increased(P<0.05), the renal tissue showed significant pathological damage, with the kidney injury molecule-1(KIM-1), neutrophil gelatinase-associated lipocalin(NGAL), and pro-apoptotic protein Bax significantly upregulated(P<0.05), while the anti-apoptotic protein Bcl-2 was significantly downregulated (P<0.05). Compared to the control or sham group, the Cis-AKI group showed a significant downregulation of SFXN4 (P<0.05); The SFXN4 and SFXN5 subtypes were significantly downregulated in the IR-AKI group and Cis-CKD group (P<0.05); All five subtypes of SFXN in the IR-CKD group were significantly downregulated (P<0.05). Conclusions Cis or IR induces renal tissue damage and tubular mitochondrial injury in mice and affects the expression of SFXN family proteins, suggesting their potential role in renal injury of animal models.

Key words: cisplatin, ischemia reperfusion, acute kidney injury, chronic kidney disease, sideroflexins

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