Abstract: TH-PO0416
Inhibition of Ferroptosis Exerts Renoprotective Effects in Membranous Nephropathy Rats via the Nrf2/HO-1 Pathway
Session Information
- Glomerular Diseases: Autoimmune Diseases
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology
Authors
- Shi, Xiujie, Beijng Huaxin Hospital First Hospital of Tsinghua University, Beijing, China
- Chang, Meiying, Beijng Huaxin Hospital First Hospital of Tsinghua University, Beijing, China
- Chen, Hanchen, Beijng Huaxin Hospital First Hospital of Tsinghua University, Beijing, China
- Tuerxun, Xierzhati, Beijng Huaxin Hospital First Hospital of Tsinghua University, Beijing, China
- Shi, Zhenwei, Beijng Huaxin Hospital First Hospital of Tsinghua University, Beijing, China
Background
This study investigated whether the nuclear factor-erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway mediates membranous nephropathy (MN) progression via ferroptosis.
Methods
A passive Heymann nephritis rat model was established by tail vein injection of anti-Fx1A. The rats were treated with ferrostatin-1 (Fer-1), the ferroptosis inhibitor, and the Nrf2 inhibitor ML385 for 2 weeks. After treatment, 24-h urine protein samples were collected along with blood and renal tissue samples.
Results
The passive Heymann nephritis rat model exhibited massive proteinuria, hypoalbuminemia, and hyperlipidemia. Fer-1 reduced proteinuria, alleviated pathological damage to renal tissues, inhibited lipid peroxidation and iron deposition, suppressed ferroptosis in renal tissues, and restored the expression of Nrf2 and HO-1. Furthermore, when the Nrf2 inhibitor ML385 was combined with Fer-1, the inhibition of Nrf2 exacerbated proteinuria, worsened renal tissue pathological damage, increased lipid peroxidation and iron deposition, and aggravated ferroptosis.
Conclusion
These findings demonstrated that ferroptosis inhibition alleviates renal injury in MN by activating the Nrf2/HO-1 pathway, suggesting a potential therapeutic target for this disease.
Funding
- Private Foundation Support