Evidence map›Paper›PMID 36010591›Full record

ReviewCells2022

Autophagy, Acute Pancreatitis and the Metamorphoses of a Trypsinogen-Activating Organelle.

Svetlana Voronina, Michael Chvanov, Francesca De Faveri, Ulrike Mayer, Tom Wileman, David Criddle, Alexei Tepikin

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
8.9field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Review
  3. Acute pancreatitis: mechanisms and therapeutic approaches.Signal transduction and targeted therapy · 2026
    Review
  4. Article
  5. Review
  6. Review
  7. Roles of chemokines in pancreatitis: A review.World journal of gastrointestinal pathophysiology · 2025
    Review
  8. Pancreatic involvement inMolecular genetics and metabolism reports · 2025
    Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. World journal of gastroenterology · 2024
    Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Svetlana VoroninaDepartment of Molecular Physiology and Cell Signalling, University of Liverpool, Liverpool L69 3BX, UK.
Michael ChvanovDepartment of Molecular Physiology and Cell Signalling, University of Liverpool, Liverpool L69 3BX, UK.ORCID 0000-0003-1747-650X
Francesca De FaveriDepartment of Molecular Physiology and Cell Signalling, University of Liverpool, Liverpool L69 3BX, UK.ORCID 0000-0001-7691-5635
Ulrike MayerBiomedical Research Centre, School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK.
Tom WilemanQuadram Institute Bioscience and Norwich Medical School, University of East Anglia, Norwich NR4 7UQ, UK.
David CriddleDepartment of Molecular Physiology and Cell Signalling, University of Liverpool, Liverpool L69 3BX, UK.
Alexei TepikinDepartment of Molecular Physiology and Cell Signalling, University of Liverpool, Liverpool L69 3BX, UK.
University of Liverpool · GBUniversity of East Anglia · GB

Funding

Medical Research Council MR/K012967/1Medical Research Council MR/N011384/1Medical Research Council MR/T002220/1Wellcome Trust 102381/Z/13/ZWellcome Trust 105273/Z/14/A
6 · The paper itself

Abstract

Recent studies have highlighted the importance of autophagy and particularly non-canonical autophagy in the development and progression of acute pancreatitis (a frequent disease with considerable morbidity and significant mortality). An important early event in the development of acute pancreatitis is the intrapancreatic activation of trypsinogen, (i.e., formation of trypsin) leading to the autodigestion of the organ. Another prominent phenomenon associated with the initiation of this disease is vacuolisation and specifically the formation of giant endocytic vacuoles in pancreatic acinar cells. These organelles develop in acinar cells exposed to several inducers of acute pancreatitis (including taurolithocholic acid and high concentrations of secretagogues cholecystokinin and acetylcholine). Notably, early trypsinogen activation occurs in the endocytic vacuoles. These trypsinogen-activating organelles undergo activation, long-distance trafficking, and non-canonical autophagy. In this review, we will discuss the role of autophagy in acute pancreatitis and particularly focus on the recently discovered LAP-like non-canonical autophagy (LNCA) of endocytic vacuoles.

Indexed as

PancreatitisTrypsinogenAcute DiseaseAutophagyHumansVacuolesTrypsinogenacute pancreatitisATG8autophagyCASMcholecystokininendocytic vacuoleLAPLAP-like non-canonical autophagyLC3LC3-associated phagocytosisLNCAnon-canonical autophagypancreatic acinar celltrypsintrypsinogenzymogen granule

Identifiers

PMID36010591
PMCPMC9406838
OpenAlexW4291366984

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.