ArticleScientific reports2017
Development of a novel model of hypertriglyceridemic acute pancreatitis in mice.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Zinc Transporter ZIP7 Is Associated with Intestinal Barrier Injury in Severe Acute Pancreatitis: Potential Roles in Mitochondrial Homeostasis and Ferroptosis.Digestive diseases and sciences · 2026Article
- Integrated Transcriptomics and Lipidomics Identify CES1-Mediated Maladaptive Lipolysis as a Key Target of Hyperlipidemic Acute Pancreatitis.Metabolites · 2026Article
- Phenyllactic Acid Restores Intestinal Epithelial Barrier to Alleviate Hypertriglyceridemic Acute Pancreatitis via a PPARγ-Dependent Mechanism.Antioxidants (Basel, Switzerland) · 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
- Potential influence of gut microbiota on the process of hypertriglyceridemia-aggravated acute pancreatitis.World journal of gastroenterology · 2026Review
- Differences in clinical features and prognosis between hypertriglyceridemia and other causes of acute pancreatitis: a dual perspective based on metabolic disorders and inflammatory response.Frontiers in endocrinology · 2026Article
- The Role of Macrophages in Acute Pancreatitis: From Inflammatory Drivers to Therapeutic Targets.International journal of medical sciences · 2026Review
- Article
- Annexin A1 mRNA-loaded liposomes alleviate acute pancreatitis by suppressing STING pathway and promoting efferocytosis in macrophages.Nature nanotechnology · 2025Article
- Acute pancreatitis experimental models, advantages and disadvantages.Journal of physiology and biochemistry · 2025Review
- Annexin A1 regulates inflammatory-immune response and reduces pancreatic and extra- pancreatic injury during severe acute pancreatitis.Genes and immunity · 2025Article
- Proton pump inhibitor use and pancreatic risk: evidence from the UK biobank participants and animal experiments.Frontiers in pharmacology · 2025Article
- Oxidative stress, DAMPs, and immune cells in acute pancreatitis: molecular mechanisms and therapeutic prospects.Frontiers in immunology · 2025Review
- Nanoparticles Fueled by Enzyme for the Treatment of Hyperlipidemic Acute Pancreatitis.ACS biomaterials science & engineering · 2024Article
- Prospective observational study and mechanistic evidence showing lipolysis of circulating triglycerides worsens hypertriglyceridemic acute pancreatitis.The Journal of clinical investigation · 2024Observational
- Apolipoprotein C-III itself stimulates the Syk/cPLA2-induced inflammasome activation of macrophage to boost anti-tumor activity of CD8Cancer immunology, immunotherapy : CII · 2023Article
- Comprehensive review on the pathogenesis of hypertriglyceridaemia-associated acute pancreatitis.Annals of medicine · 2023Review
- Neddylation-mediated degradation of hnRNPA2B1 contributes to hypertriglyceridemia pancreatitis.Cell death & disease · 2022Article
- Hypertriglyceridemia Acute Pancreatitis: Animal Experiment Research.Digestive diseases and sciences · 2022Review
- A Severe Acute Pancreatitis Mouse Model Transited from Mild Symptoms Induced by a "Two-Hit" Strategy with L-Arginine.Life (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
15 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The morbidity rate of hypertriglyceridemic acute pancreatitis (HTG-AP) increased rapidly over the last decade. However an appropriate animal model was lacking to recapitulate this complicated human disease. We established a novel mice model of HTG-AP by poloxamer 407 (P-407) combined with caerulein (Cae). In our study, serum triglyceride levels of P-407 induced mice were elevated in a dose-dependent manner, and the pancreatic and pulmonary injuries were much severer in HTG mice than normal mice when injected with conventional dose Cae (50 ug/kg), what's more, the severity of AP was positively correlative with duration and extent of HTG. In addition, we found that a low dose Cae (5 ug/kg) could induce pancreatic injury in HTG mice while there was no obvious pathological injury in normal mice. Finally, we observed that HTG leaded to the increased infiltrations of macrophages and neutrophils in mice pancreatic tissues. In conclusion, we have developed a novel animal model of HTG-AP that can mimic physiological, histological, clinical features of human HTG-AP and it could promote the development of therapeutic strategies and advance the mechanism research on HTG-AP.
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