ArticleBMC gastroenterology2024
Autophagy-mediated ferroptosis is involved in development of severe acute pancreatitis.
Article in BMC gastroenterology, 2024. 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.
- SOX4 Knockdown Represses Pancreatic Acinar Cells Ferroptosis in Acute Pancreatitis Through Reducing LPCAT3 Expression.Digestive diseases and sciences · 2026Article
- circ-FSCN1 affects ferroptosis and cell viability in NSCLC via the miR-506-3p/SLC7A1 pathway.Translational oncology · 2026Article
- Obesity suppresses neutrophil-dependent itaconate signaling promoting ferroptosis in acute pancreatitis.Redox biology · 2026Article
- Homoplantaginin protects pancreatic tissue in severe acute pancreatitis mice via inhibiting ferroptosis by modulating the circDNMT3B/miR-20b-5p/SLC7A11 axis.BMC gastroenterology · 2026Article
- Therapeutic potential of plant polyphenols in acute pancreatitis.Inflammopharmacology · 2025Review
- Epithelial-Mesenchymal Transition Suppression by ML210 Enhances Gemcitabine Anti-Tumor Effects on PDAC Cells.Biomolecules · 2025Article
- Ferroptosis in Hypertriglyceridemic Acute Pancreatitis: Mechanisms and Therapeutic Implications.Journal of inflammation research · 2025Review
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Authors and funding
7 authors.
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Abstract
backgroundFerroptosis is a newly recognized form of regulatory cell death characterized by severe lipid peroxidation triggered by iron overload and the production of reactive oxygen species (ROS). However, the role of ferroptosis in severe acute pancreatitis(SAP) has not been fully elucidated.
methodsWe established four severe acute pancreatitis models of rats including the sham control group, the SAP group, the Fer -1-treated SAP (SAP + Fer-1) group, the 3-MA-treated SAP (SAP + 3-MA) group. The SAP group was induced by retrograde injection of sodium taurocholate into the pancreatic duct. The other two groups were intraperitoneally injected with ferroptosis inhibitor (Fer-1) and autophagy inhibitor (3-MA), respectively. The model of severe acute pancreatitis with amylase crest-related inflammatory factors was successfully established. Then we detected ferroptosis (GPX4, SLC7A1 etc.) and autophagy-related factors (LC3II, p62 ect.) to further clarify the relationship between ferroptosis and autophagy.
resultsOur study found that ferroptosis occurs during the development of SAP, such as iron and lipid peroxidation in pancreatic tissues, decreased levels of reduced glutathione peroxidase 4 (GPX 4) and glutathione (GSH), and increased malondialdehyde(MDA) and significant mitochondrial damage. In addition, ferroptosis related proteins such as GPX4, solute carrier family 7 member 11(SLC7A11) and ferritin heavy chain 1(FTH1) were significantly decreased. Next, the pathogenesis of ferroptosis in SAP was studied. First, treatment with the ferroptosis inhibitor ferrostatin-1(Fer-1) significantly alleviated ferroptosis in SAP. Interestingly, autophagy occurs during the pathogenesis of SAP, and autophagy promotes the occurrence of ferroptosis in SAP. Moreover, 3-methyladenine (3-MA) inhibition of autophagy can significantly reduce iron overload and ferroptosis in SAP.
conclusionsOur results suggest that ferroptosis is a novel pathogenesis of SAP and is dependent on autophagy. This study provides a new theoretical basis for the study of SAP.
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