ArticleScientific reports2023
Ferroptosis is involved in focal segmental glomerulosclerosis in rats.
Article in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 6 citations in OpenAlex.
- Single-cell transcriptomics and machine-learning reveal M1 macrophage-driven progression from minimal change disease to focal segmental glomerulosclerosis.Renal failure · 2026Article
- Eugenol Mitigates Mercuric Chloride-Induced Renal Injury by Attenuating Oxidative Stress, Ferroptosis, ER Stress, Apoptosis, and Autophagy.Biological trace element research · 2026Article
- Hyperbaric Oxygen Therapy - a Potential Therapy for Macro- and Trace Elements' Imbalance in Patients with Chronic Kidney Disease?Biological trace element research · 2026Article
- Protective Effect of Chinese Herbal Medicine on Cerebral Ischemia-Reperfusion Injury by Regulating Ferroptosis.Drug design, development and therapy · 2026Review
- Curculigoside alleviates ferroptosis in renal interstitial fibrosis by regulating the Nrf2/HO-1 signaling pathway.American journal of translational research · 2025Article
- Unraveling Ferroptosis: A New Frontier in Combating Renal Fibrosis and CKD Progression.Biology · 2024Review
- Increased ER stress by depletion of PDIA6 impairs primary ciliogenesis and enhances sensitivity to ferroptosis in kidney cells.BMB reports · 2024Article
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Authors and funding
9 authors at 2 institutions in 1 country.
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Abstract
To explore whether ferroptosis is involved in focal segmental glomerulosclerosis (FSGS) and its mechanism. The FSGS rat model was constructed by single nephrectomy combined with fractional tail vein injection of doxorubicin. 24-hour urine protein, serum biochemistry, HE, PAS and Masson pathological staining were measured to assess renal injury. Glomerular and morphological changes of ferroptosis were observed by transmission electron microscopy. Iron content in renal tissue was assessed by Prussian blue staining and iron detection. GSH/GSSG kit was used to detect the content and proportion of reduced/oxidized glutathione. Lipid peroxidation related proteins including MDA expression was assessed by colorimetry. The iron metabolism biomarkers such as hepcidin, ferroportin and TFR, ferroptosis biomarkers such as GPX4, ACSL4, and ferritinophagy biomarkers such as LC3II/LC3I, NCOA4, and FTH1 were detected by Western blot. Significant urinary protein, hyperlipidemia, azotemia, increased serum creatinine and hypoproteinemia were observed in FSGS rats. Histology and electron microscopy showed segmental sclerosis of glomeruli, compensatory enlargement of some glomeruli, occlusion of capillary lumen, balloon adhesion, increased mesangial matrix, atrophy of some tubules, and renal interstitial fibrosis in renal tissue of FSGS rats. The morphology of glomerular foot processes disappeared; the foot processes were extensively fused and some foot processes detached. Mitochondria became smaller, membrane density increased, and mitochondrial cristae decreased or disappeared. In addition, iron deposition was observed in renal tissue of FSGS rats. Compared with the control group, the levels of GSH, GSH/GSSG, GPX4, and ferroportin were reduced and the expression of GSSG, MDA, ACSL4, hepcidin, and TFR was increased in the renal tissue of FSGS rats; meanwhile, the expression of LC3II/LC3I and NCOA4 was increased and the expression of FTH1 was decreased. Ferroptosis is involved in the pathological progression of FSGS, which is probably associated with activation of ferritinophagy. This represents a potential therapeutic target for FSGS.
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