ReviewDer Internist2021
[Pathogenesis of acute pancreatitis].
Review in Der Internist, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Autophagy dysfunction in pancreatic acinar cells in acute pancreatitis: from molecular mechinery and trypsinogen activation to heterogeneity and therapeutic implications.Journal of molecular histology · 2026Review
- Structural insight into the CUB2 domain's role in enteropeptidase-mediated trypsinogen activation.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Review
- Homoplantaginin protects pancreatic tissue in severe acute pancreatitis mice via inhibiting ferroptosis by modulating the circDNMT3B/miR-20b-5p/SLC7A11 axis.BMC gastroenterology · 2026Article
- Traditional Chinese medicine in pancreatitis: mechanisms, integrative strategies, and clinical perspectives.Frontiers in medicine · 2026Review
- Roles of chemokines in pancreatitis: A review.World journal of gastrointestinal pathophysiology · 2025Review
- Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosisWorld journal of gastroenterology · 2025Article
- CLDN4 promotes ferroptosis and inflammation involving JAK2/STAT3 pathway in acute pancreatitis.Functional & integrative genomics · 2025Article
- Systemic Bile Acids Affect the Severity of Acute Pancreatitis in Mice Depending on Their Hydrophobicity and the Disease Pathogenesis.International journal of molecular sciences · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute pancreatitis is characterized by the autodigestion of the pancreas by its own digestive enzymes. The pathophysiological onset of the disease occurs in the acinar cells. The normally inactive precursors of secreted proteases are prematurely activated and as a result digest the cells from within. The activation of trypsinogen to trypsin represents the key event as active trypsin activates further digestive enzymes and can therefore initiate the activation of the complete protease cascade. This premature activation of proteases results in the cell death of acinar cells and in the induction of a strong proinflammatory immune response. Cells of the innate immune system migrate into the damaged organ and potentiate the local damage again via the release of inflammatory cytokines, such as tumor necrosis factor alpha and reactive oxygen species. Concomitant to the local immune reaction, a systemic activation of the immune system also occurs, which can develop into a systemic inflammatory response syndrome (SIRS). In the course of the SIRS severe complications such as organ failure can occur. The consequence of this pronounced SIRS in the later course of the disease is a strong immunological counter-regulation, the so-called compensatory anti-inflammatory reaction syndrome (CARS). In the course of this immunosuppression commensal bacteria from the intestines can colonize the pancreatic necrosis. The outcome of the SIRS/CARS balance is decisive for the course and the prognosis of the patient.
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What OpenQuestion holds
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.