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Ferroptosis is involved in passive Heymann nephritis in rats
Xiujie Shi1, Qi Zhang1, Meiying Chang1
1Department of Nephrology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing, 100091, China.
Abstract:
Ferroptosis is found to be involved in some experimental models of kidney diseases, but its role in membrane nephropathy (MN) is still unclear. The purpose of this study is to explore whether ferroptosis occurred in MN, and the role of ferritinophagy. In this study, passive Heymann nephritis (PHN) rats were induced by single tail vein injection of anti-Fx1A serum, and normal rats were used as control. The changes of 24 h urinary protein, serum biochemical parameters, renal pathological damage, iron content, lipid peroxidation parameters, ferroptosis markers, and ferritinophagy markers were evaluated in the two groups. Compared with the control group, PHN rats showed obvious proteinuria, hypoproteinemia, and hyperlipidemia. Besides, more severe renal pathological damage and higher Fe2+ levels were observed in PHN rats, and the levels of malondialdehyde (MDA) increased significantly, while the levels of superoxide Dismutase (SOD) and glutathione (GSH) decreased. In addition, the expression of glutathione peroxidase 4 (GPX4) in renal tissues of PHN rats decreased significantly, while the expression of transferrin receptor (TFR) and acyl-CoA synthetase long-chain family member 4 (ACSL4) increased. The expression of microtubule associated protein 1 light chain 3 (LC3) II/LC3I and nuclear receptor coactivator 4 (NCOA4) increased significantly. Therefore, our study shows that ferroptosis is involved in the pathological damage of MN, and companied by activation of ferritinophagy.
Insights
Ferroptosis, a cell death process, is implicated in membranous nephropathy (MN) kidney disease. This study found increased ferroptosis and ferritinophagy in MN rats, suggesting their role in disease progression.
Area of Science:
- Nephrology
- Cell Biology
- Pathology
Background:
- Ferroptosis involvement in kidney diseases is known, but its role in membranous nephropathy (MN) remains unclear.
- Understanding ferroptosis and ferritinophagy in MN is crucial for developing targeted therapies.
Purpose of the Study:
- To investigate the occurrence of ferroptosis in a rat model of membranous nephropathy (MN).
- To explore the role of ferritinophagy in the pathological mechanisms of MN.
Main Methods:
- Passive Heymann nephritis (PHN) was induced in rats.
- Evaluated urinary protein, serum biochemistry, renal pathology, iron levels, lipid peroxidation, ferroptosis, and ferritinophagy markers.
Main Results:
- PHN rats exhibited proteinuria, hypoproteinemia, hyperlipidemia, and severe renal damage.
- Increased iron (Fe2+), malondialdehyde (MDA), transferrin receptor (TFR), acyl-CoA synthetase long-chain family member 4 (ACSL4), LC3 II/I, and nuclear receptor coactivator 4 (NCOA4) were observed.
- Decreased superoxide Dismutase (SOD), glutathione (GSH), and glutathione peroxidase 4 (GPX4) indicated ferroptosis activation.
Conclusions:
- Ferroptosis is actively involved in the renal pathological damage associated with membranous nephropathy (MN).
- Ferritinophagy activation accompanies ferroptosis, suggesting a combined role in MN pathogenesis.
