Abstract: SA-PO0254
Exploration of Cellular Characteristics and Potential Ferroptosis-Related Genes in Contrast-Induced Nephropathy Based on Single-Cell RNA Sequencing
Session Information
- AKI: Mechanisms - Cell Signaling
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Acute Kidney Injury
- 103 AKI: Mechanisms
Authors
- Guo, Zhenyu, Ningbo No.2 Hospital, Ningbo, China
- Zhou, Fangfang, Ningbo No.2 Hospital, Ningbo, China
- Luo, Qun, Ningbo No.2 Hospital, Ningbo, China
Background
This study aims to investigate the changes in cell types, differences in gene expression, and potential molecular mechanisms underlying the pathogenesis of contrast-induced nephropathy through single-cell RNA sequencing analysis, with a particular focus on the correlation with ferroptosis mechanisms.
Methods
C57 mice were divided into Group control: blank control group (n=2), Group CIN+Fer-1: contrast agent nephropathy + ferroptosis inhibitor group (n=3), and Group CIN: contrast agent nephropathy model group (n=3). Using 10x Genomics single-cell transcriptome sequencing technology, a large number of cells from the three sample groups were captured and analyzed to obtain sequencing data. Data quality assessment confirmed the reliability of the data.
Results
The proportion of proximal tubule (PT) cells significantly increased, identifying PT as the primary site of contrast-induced injury. Heatmaps of marker gene expression across different cell types revealed relatively higher expression levels of ferroptosis-related genes (e.g., Gpx4, Gclc, Ptgs2, Mafg) in PT cells, suggesting that proximal tubule cells inherently exhibit elevated expression of ferroptosis-related genes. KEGG pathway enrichment analysis demonstrated significant enrichment of the peroxisome pathway in PT cells, implying that this cell type may become a major target of ferroptosis due to dysregulated lipid metabolism and oxidative stress imbalance . In the CIN model, PT cells exhibited downregulated ferroptosis-suppressing genes (Gpx4, Gclc, Fth1, Lamp2) and upregulated pro-ferroptosis genes (Nox4, Mafg, Ptgs2). Fer-1 intervention restored Gpx4/Gclc expression and inhibited Nox4 upregulation, effectively reversing the ferroptosis-related profile in PT cells.
Conclusion
Ferroptosis inhibitors may exert a protective effect against contrast-induced nephropathy. The specific mechanism may involve regulating cellular composition and suppressing the expression of ferroptosis-related genes. This provides crucial molecular evidence and a research foundation for further understanding the pathogenesis of contrast-induced nephropathy and the role of ferroptosis in this process.