Evidence map›Paper›PMID 22885948›Full record

ReviewCurrent opinion in gastroenterology2012

Pathogenic mechanisms of acute pancreatitis.

Raghuwansh P Sah, Pramod Garg, Ashok K Saluja

Abstract readReview
In one paragraph

Review in Current opinion in gastroenterology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed, 2 pooled it
–field-weighted citation impact
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

79 citing papers in PubMed, 2 syntheses or guidelines pooled it.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Review
  5. Article
  6. Methanol Extract fromAntioxidants (Basel, Switzerland) · 2025
    Article
  7. Article
  8. Review
  9. Article
  10. Biological and Molecular Characterization of FiveTropical medicine and infectious disease · 2025
    Article
  11. Article
  12. DGA ameliorates severe acute pancreatitis through modulating macrophage pyroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  13. The TRIM28/miR133a/CD47 axis acts as a potential therapeutic target in pancreatic necrosis by impairing efferocytosis.Molecular therapy : the journal of the American Society of Gene Therapy · 2024
    Article
  14. Review
  15. Interleukins: pathophysiological role in acute pancreatitis.Archives of medical science : AMS · 2024
    Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Article

19 more citing papers are in PubMed but not listed here.

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

3 authors.

Raghuwansh P SahDepartment of Surgery, University of Minnesota, Minneapolis, Minnesota, USA.
Pramod Garg
Ashok K Saluja

Funding

HEAT SHOCK PROTEINS AND PANCREATITISR01DK058694 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI RAMAKRISHNAN, SUNDARAM · 2001 to 2019
$5.4M
Relative Contribution of Trypsin & Inflammation in Acute & Chronic PancreatitisR01DK093047 · NIDDK · UNIVERSITY OF MINNESOTA · PI DAWRA, RAJINDER K · 2011 to 2021
$5.0M
The Inhibition of HSP70 Induces Apoptosis in Pancreatic Cancer CellsR01CA124723 · NCI · UNIVERSITY OF MINNESOTA · PI GILBOA, ELI, RAMAKRISHNAN, SUNDARAM · 2007 to 2022
$4.5M
Physiology and pathophysiology of human pancreatic acinar cellsR01DK092145 · NIDDK · UNIVERSITY OF MINNESOTA · PI SALUJA, ASHOK K · 2011 to 2014
$1.4M
NCI NIH HHS R01 CA124723NIDDK NIH HHS R01 DK058694NIDDK NIH HHS R01 DK092145NIDDK NIH HHS R01 DK093047
6 · The paper itself

Abstract

purpose of reviewIn this article, recent advances in the pathogenesis of acute pancreatitis have been reviewed. RECENT

findingsPathologic intra-acinar trypsinogen activation had been hypothesized to be the central mechanism of pancreatitis for over a century. This hypothesis could be explored for the first time with the development of a novel mouse model lacking pathologic intra-acinar trypsinogen activation. It became clear that intra-acinar trypsinogen activation contributes to early acinar injury, but local and systemic inflammation progress independently during pancreatitis. Early intra-acinar nuclear factor kappa B (NFκB) activation, which occurs parallel to but independent of trypsinogen activation, may be crucial in pancreatitis. Although the mechanism of NFκB and trypsinogen activation is not entirely clear, further insights have been made into key pathogenic cellular events such as calcium signaling, mitochondrial dysfunction, endoplasmic reticulum (ER) stress, autophagy and impaired trafficking, and lysosomal and secretory responses. Cellular intrinsic damage-sensing mechanisms that lead to activation of the inflammatory response aimed at repair, but lead to disease when overwhelmed, are beginning to be understood. SUMMARY: New findings necessitate a paradigm shift in our understanding of acute pancreatitis. Intra-acinar trypsinogen activation leads to early pancreatic injury, but the inflammatory response of acute pancreatitis develops independently, driven by early activation of inflammatory pathways.

Indexed as

Acinar CellsAnimalsAutophagyCalciumHumansInflammasomesMitochondriaNF-kappa BPancreatitisTrypsinogenCalciumInflammasomesNF-kappa BTrypsinogen

Identifiers

PMID22885948
PMCPMC3682674

What OpenQuestion holds

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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 OpenQuestion graph.