ReviewAmerican journal of physiology. Gastrointestinal and liver physiology2026
Pathologically relevant trypsinogen activation in pancreatitis.
Review in American journal of physiology. Gastrointestinal and liver physiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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Who cites it
4 citing papers in PubMed.
- Marine-Derived Proteins: Individual Variability in Health Effects Across Protein Structure, Host Genetics, and Gut Microbiota.Comprehensive reviews in food science and food safety · 2026Review
- Protease-Activated Receptor-2 as a Proteolytic Rheostat in Colorectal and Pancreatic Cancer: From Mechanism to Biomarker-Guided Therapy.International journal of molecular sciences · 2026Review
- Intraductal digestive enzyme accumulation drives lethal hemorrhagic necrotizing pancreatitis and enables therapeutic intervention.Research square · 2026Article
- Pancreatitis-associated chymotrypsin C (CTRC) variant p.R240Q selectively impairs trypsinogen degradation through disruption of long-range electrostatic interactions.Scientific reports · 2026Article
Corrections and comments
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Authors and funding
1 author.
Funding
Abstract
Pancreatitis is an inflammatory disorder of the pancreas that occurs in acute, recurrent acute, and chronic forms, often leading to severe complications and long-term functional impairment. The disease develops through multiple pathological mechanisms, including the premature activation of the digestive proenzyme trypsinogen within the pancreas. Conversion of trypsinogen to its active form trypsin may be catalyzed by the lysosomal protease cathepsin B or may occur through autoactivation, a self-amplifying reaction in which trypsin activates trypsinogen. Accumulating evidence from genetic, biochemical, and animal model studies on trypsinogen mutations associated with human pancreatitis strongly supports autoactivation as a key driver of disease pathogenesis, whereas cathepsin B-mediated activation may play a context-dependent, lesser role. This review explores the biochemical pathways of intrapancreatic trypsinogen activation and discusses their respective contributions to the multifactorial pathogenesis of pancreatitis.
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Registered trials
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