ReviewCurrent opinion in gastroenterology2013
New insights into the pathogenesis of pancreatitis.
Review in Current opinion in gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 3 of them syntheses that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
86 citing papers in PubMed, 3 syntheses or guidelines pooled it, 179 citations in OpenAlex.
- Meta-analysis and field synopsis of genetic variants associated with the risk and severity of acute pancreatitis.BJS open · 2020Pooled it
- Pharmacological interventions for acute pancreatitis.The Cochrane database of systematic reviews · 2017Pooled it
- Interventions for necrotising pancreatitis.The Cochrane database of systematic reviews · 2016Pooled it
- Prevention of Severe Acute Pancreatitis With Cyclooxygenase-2 Inhibitors: A Randomized Controlled Clinical Trial.The American journal of gastroenterology · 2020Trial
- A Novel Insight into Chronic Pancreatitis Pathogenesis: the USP1/ITGB5 Axis-Mediated Stellate Cell Activation.Inflammation · 2026Article
- Nano-Reagents in Acute Pancreatitis: Diagnostic, Therapeutic, and Theranostic Advances.International journal of nanomedicine · 2026Review
- Article
- Targeting Oxidative Stress in Acute Pancreatitis: A Critical Review of Antioxidant Strategies.Nutrients · 2025Review
- Article
- Gene Regulation of Neutrophils Mediated Liver and Lung Injury through NETosis in Acute Pancreatitis.Inflammation · 2025Article
- Efficacy of Xuebijing injection on pulmonary ventilation improvement in acute pancreatitis: a systematic review and meta-analysis.Frontiers in pharmacology · 2025Review
- Trypsin in pancreatitis: The culprit, a mediator, or epiphenomenon?World journal of gastroenterology · 2024Review
- Acute pancreatitis as a risk factor of chronic pancreatitis and pancreatic cancer. An overview.Biomedical papers of the Medical Faculty of the University Palacky, Olomouc, Czechoslovakia · 2024Review
- Recent insights about autophagy in pancreatitis.eGastroenterology · 2024Article
- Repetitive Cerulein-Induced Chronic Pancreatitis in Growing Pigs-A Pilot Study.International journal of molecular sciences · 2023Article
- Surgical management of acute pancreatitis: Historical perspectives, challenges, and current management approaches.World journal of gastrointestinal surgery · 2023Review
- Piezo1-mediated stellate cell activation causes pressure-induced pancreatic fibrosis in mice.JCI insight · 2022Article
- The diverse roles of TMEM16A CaJournal of advanced research · 2021Review
- Targeting purinergic receptors to suppress the cytokine storm induced by SARS-CoV-2 infection in pulmonary tissue.International immunopharmacology · 2021Review
- Clinical feature of severe fever with thrombocytopenia syndrome (SFTS)-associated encephalitis/encephalopathy: a retrospective study.BMC infectious diseases · 2021Article
26 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
purpose of reviewIn this article, we review important advances in our understanding of the mechanisms of pancreatitis. RECENT
findingsThe relative contributions of intrapancreatic trypsinogen activation and nuclear factor kappa B (NFκB) activation, the two major early independent cellular events in pancreatitis, have been investigated using novel genetic models. Trypsinogen activation has traditionally held the spotlight for many decades as the central pathogenic event of pancreatitis. However, recent experimental evidence points to the role of trypsin activation in early acinar cell damage but not in the inflammatory response of acute pancreatitis, which was shown to be induced by NFκB activation. Further, chronic pancreatitis developed independently of trypsinogen activation in the caerulein model. Sustained NFκB activation, but not persistent intra-acinar expression of active trypsin, was shown to result in chronic pancreatitis. Calcineurin-NFAT (nuclear factor of activated T-cells) signaling was shown to mediate downstream effects of pathologic rise in intracellular calcium. Interleukin-6 was identified as a key cytokine mediating pancreatitis-associated lung injury. SUMMARY: Recent advances challenge the long-believed trypsin-centered understanding of pancreatitis. It is becoming increasingly clear that activation of intense inflammatory signaling mechanisms in acinar cells is crucial to the pathogenesis of pancreatitis, which may explain the strong systemic inflammatory response in pancreatitis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.