ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2019
Elevated intracellular trypsin exacerbates acute pancreatitis and chronic pancreatitis in mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 39 citations in OpenAlex.
- IL-18 promotes pancreatic fibrosis via release of IL-4 from pancreatic stellate cells and induces macrophage M2 polarization.Scientific reports · 2026Article
- Acute pancreatitis experimental models, advantages and disadvantages.Journal of physiology and biochemistry · 2025Review
- Development and validation of dynamic clinical subphenotypes in acute pancreatitis patients using vital sign trajectories in intensive care units: a multinational cohort study.Signal transduction and targeted therapy · 2025Article
- Deletion of the WD40 domain of ATG16L1 exacerbates acute pancreatitis, abolishes LAP-like non-canonical autophagy and slows trypsin degradation.Autophagy · 2025Article
- Therapeutic potential of traditional Chinese medicine in pancreatic fibrosis: mechanisms of TCM formulas and active ingredients.Frontiers in pharmacology · 2025Review
- Enzyme Inhibitory, Physicochemical, and Phytochemical Properties and Botanical Sources of Honey, Bee Pollen, Bee Bread, and Propolis Obtained from the Same Apiary.Antioxidants (Basel, Switzerland) · 2024Article
- Albiflorin Alleviates Severe Acute Pancreatitis-Associated Liver Injury by Inactivating P38MAPK/NF-κB Signaling Pathway.Biochemical genetics · 2024Article
- Trypsin in pancreatitis: The culprit, a mediator, or epiphenomenon?World journal of gastroenterology · 2024Review
- Identification and analysis of chemokine-related and NETosis-related genes in acute pancreatitis to develop a predictive model.Frontiers in genetics · 2024Article
- Interleukin‑22 alleviates arginine‑induced pancreatic acinar cell injury via the regulation of intracellular vesicle transport system: Evidence from proteomic analysis.Experimental and therapeutic medicine · 2023Article
- MLKL signaling regulates macrophage polarization in acute pancreatitis through CXCL10.Cell death & disease · 2023Article
- Comprehensive review on the pathogenesis of hypertriglyceridaemia-associated acute pancreatitis.Annals of medicine · 2023Review
- Diagnostic Potential of Ratio Between Creatine Kinase and Amylase in Acute Pancreatitis.Materia socio-medica · 2023Article
- The Rabep1-Mediated Endocytosis and Activation of Trypsinogen to Promote Pancreatic Stellate Cell Activation.Biomolecules · 2022Article
- Expression of serum autophagy-related protein P62 in patients with severe pancreatitis and its correlation with prognosis.American journal of translational research · 2022Article
- CaMK II Inhibition Attenuates ROS Dependent Necroptosis in Acinar Cells and Protects against Acute Pancreatitis in Mice.Oxidative medicine and cellular longevity · 2021Article
- A narrative review of acute pancreatitis and its diagnosis, pathogenetic mechanism, and management.Annals of translational medicine · 2021Review
- Drug discovery and formulation development for acute pancreatitis.Drug delivery · 2020Review
- A Paper-Based Near-Infrared Optical Biosensor for Quantitative Detection of Protease Activity Using Peptide-Encapsulated SWCNTs.Sensors (Basel, Switzerland) · 2020Article
- The Use of Values WNR and GNR to Distinguish between and Diagnose Different Types of Pancreatitis.Molecular therapy. Methods & clinical development · 2020Article
Corrections and comments
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Authors and funding
14 authors at 7 institutions in 2 countries.
Funding
Abstract
Intra-acinar trypsinogen activation occurs in the earliest stages of pancreatitis and is believed to play important roles in pancreatitis pathogenesis. However, the exact role of intra-acinar trypsin activity in pancreatitis remains elusive. Here, we aimed to examine the specific effects of intra-acinar trypsin activity on the development of pancreatitis using a transgenic mouse model. This transgenic mouse model allowed for the conditional expression of a mutant trypsinogen that can be activated specifically inside pancreatic acinar cells. We found that expression of this active mutated trypsin had no significant effect on triggering spontaneous pancreatitis. Instead, several protective compensatory mechanisms, including SPINK1 and heat shock proteins, were upregulated. Notably, these transgenic mice developed much more severe acute pancreatitis, compared with control mice, when challenged with caerulein. Elevated tissue edema, serum amylase, inflammatory cell infiltration and acinar cell apoptosis were dramatically associated with increased trypsin activity. Furthermore, chronic pathological changes were observed in the pancreas of all transgenic mice, including inflammatory cell infiltration, parenchymal atrophy and cell loss, fibrosis, and fatty replacement. These changes were not observed in control mice treated with caerulein. The alterations in pancreata from transgenic mice mimicked the histological changes common to human chronic pancreatitis. Taken together, we provided in vivo evidence that increased intra-acinar activation of trypsinogen plays an important role in the initiation and progression of both acute and chronic pancreatitis.
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