ReviewCell death discovery2024
Ferroptosis exacerbates hyperlipidemic acute pancreatitis by enhancing lipid peroxidation and modulating the immune microenvironment.
Review in Cell death discovery, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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Who cites it
27 citing papers in PubMed.
- The Correlation Analysis of C-Reactive Protein-Triglyceride-Glucose Index with the Severity of Hyperlipidemic Acute Pancreatitis.Digestive diseases and sciences · 2026Article
- Review
- Effects of Abnormal Lipid Metabolism on Pancreatic Injury and Ferroptosis-Related Indicators in Rats with Severe Acute Pancreatitis.Digestive diseases and sciences · 2026Article
- SOX4 Knockdown Represses Pancreatic Acinar Cells Ferroptosis in Acute Pancreatitis Through Reducing LPCAT3 Expression.Digestive diseases and sciences · 2026Article
- miR-215-5p aggravates severe acute pancreatitis by inhibiting SLC7A11 to induce ferroptosis.BMC gastroenterology · 2026Article
- Fibulin-1 Improves Caerulein-Induced Acute Pancreatitis In Vitro by Inhibiting Ferroptosis.Journal of biochemical and molecular toxicology · 2026Article
- Obesity suppresses neutrophil-dependent itaconate signaling promoting ferroptosis in acute pancreatitis.Redox biology · 2026Article
- Deep chemical structure graph learning deciphers the lipotoxicity code of hypertriglyceridemic pancreatitis.NPJ digital medicine · 2026Article
- Colchicine alleviates severe acute pancreatitis in rats by inhibiting acinar cell ferroptosisEuropean journal of histochemistry : EJH · 2026Article
- Genome-wide investigations of the lipid accumulation product index pinpoints polygenic determinants underlying pancreatitis susceptibility.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Targeting ferroptosis mediated cell death: a novel strategy for mitigating acute pancreatitis.Molecular biology reports · 2026Review
- Targeting Autophagy, Ferroptosis, and Neuroinflammation: Polyphenol-Mediated Modulation of Emerging Signaling Pathways in Neurodegeneration.Molecular neurobiology · 2026Review
- Targeting mitochondrial phosphatase PGAM5 alleviates ferroptosis and acute pancreatitis by upregulating NRF2-mediated FSP1 expression.Cell death & disease · 2026Article
- Cell death and its interaction with mitochondrial dysfunction in pathogenesis of acute pancreatitis: a comprehensive review.Apoptosis : an international journal on programmed cell death · 2026Review
- Effects of low molecular weight heparin on inflammatory, coagulation, and immune markers in hyperlipidemic acute pancreatitis.Journal of medical biochemistry · 2026Article
- SCO‑792 alleviates HFD‑aggravated chronic pancreatitis by modulating the gut-pancreas axis via the AMPK/ACC and TLR4/NF‑κB signaling pathways.Frontiers in immunology · 2026Article
- Post-translational modification crosstalk in acute pancreatitis: linking acinar stress to innate immune amplification and tissue repair.Frontiers in immunology · 2026Review
- Mechanistic insights into how intrapancreatic fat deposition drives the development of acute pancreatitis.International journal of biological sciences · 2026Review
- Osmolarity trajectories and outcomes in patients with acute pancreatitis in the intensive care unit: group-based trajectory modeling.BMC medical informatics and decision making · 2025Article
- Hypertriglyceridemic pancreatitis: perspectives from China.Current opinion in gastroenterology · 2025Review
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Abnormal activation of ferroptosis worsens the severity of acute pancreatitis and intensifies the inflammatory response and organ damage, but the detailed underlying mechanisms are unknown. Compared with other types of pancreatitis, hyperlipidemic acute pancreatitis (HLAP) is more likely to progress to necrotizing pancreatitis, possibly due to peripancreatic lipolysis and the production of unsaturated fatty acids. Moreover, high levels of unsaturated fatty acids undergo lipid peroxidation and trigger ferroptosis to further exacerbate inflammation and worsen HLAP. This paper focuses on the malignant development of hyperlipidemic pancreatitis with severe disease combined with the core features of ferroptosis to explore and describe the mechanism of this phenomenon and shows that the activation of lipid peroxidation and the aberrant intracellular release of many inflammatory mediators during ferroptosis are the key processes that regulate the degree of disease development in patients with HLAP. Inhibiting the activation of ferroptosis effectively reduces the intensity of the inflammatory response, thus reducing organ damage in patients and preventing the risk of HLAP exacerbation. Additionally, this paper summarizes the key targets and potential therapeutic agents of ferroptosis associated with HLAP deterioration to provide new ideas for future clinical applications.
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