Evidence map›Paper›PMID 21875495›Full record

ArticleGastroenterology2011

Intra-acinar trypsinogen activation mediates early stages of pancreatic injury but not inflammation in mice with acute pancreatitis.

Rajinder Dawra, Raghuwansh P Sah, Vikas Dudeja, Loveena Rishi, Rupjoyti Talukdar, Pramod Garg, Ashok K Saluja

Open access · greenAbstract read
In one paragraph

Article in Gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 138 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
138citing papers in PubMed, 1 pooled it
13.3field-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

138 citing papers in PubMed, 1 synthesis or guideline pooled it, 247 citations in OpenAlex.

  1. Pooled it
  2. Role of cathepsin B in spontaneous pancreatitis in T7D23A trypsinogen mutant mice.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2026
    Article
  3. Article
  4. Article
  5. Article
  6. Pathologically relevant trypsinogen activation in pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Article
  12. Pancreatic involvement inMolecular genetics and metabolism reports · 2025
    Article
  13. Acute pancreatitis: Translating early mechanisms to bedside management.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2025
    Review
  14. Predictive Value of SerumDiagnostics (Basel, Switzerland) · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Lysine acetylation and its role in the pathophysiology of acute pancreatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
    Review
  19. Review
  20. Article

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

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Rajinder DawraDivision of Basic and Translational Research, Department of Surgery, University of Minnesota, Minneapolis, Minnesota, USA.
Raghuwansh P Sah
Vikas Dudeja
Loveena Rishi
Rupjoyti Talukdar
Pramod Garg
Ashok K Saluja
University of Minnesota · USTwin Cities Orthopedics · US

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
Physiology and pathophysiology of human pancreatic acinar cellsR01DK092145 · NIDDK · UNIVERSITY OF MINNESOTA · PI SALUJA, ASHOK K · 2011 to 2014
$1.4M
NIDDK NIH HHS R01 DK058694NIDDK NIH HHS R01 DK 092145NIDDK NIH HHS R01 DK092145NIDDK NIH HHS R01 DK093047
6 · The paper itself

Abstract

BACKGROUND &

aimsThe role of trypsinogen activation in the pathogenesis of acute pancreatitis (AP) has not been clearly established.

methodsWe generated and characterized mice lacking trypsinogen isoform 7 (T7) gene (T(-/-)). The effects of pathologic activation of trypsinogen were studied in these mice during induction of AP with cerulein. Acinar cell death, tissue damage, early intra-acinar activation of the transcription factor nuclear factor κB (NF-κB), and local and systemic inflammation were compared between T(-/-) and wild-type mice with AP.

resultsDeletion of T7 reduced the total trypsinogen content by 60% but did not affect physiologic function. T(-/-) mice lacked pathologic activation of trypsinogen, which occurs within acinar cells during early stages of AP progression. Absence of trypsinogen activation in T(-/-) mice led to near complete inhibition of acinar cell death in vitro and a 50% reduction in acinar necrosis during AP progression. However, T(-/-) mice had similar degrees of local and systemic inflammation during AP progression and comparable levels of intra-acinar NF-κB activation, which was previously shown to occur concurrently with trypsinogen activation during early stages of pancreatitis.

conclusionsT7 is activated during pathogenesis of AP in mice. Intra-acinar trypsinogen activation leads to acinar death during early stages of pancreatitis, which accounts for 50% of the pancreatic damage in AP. However, progression of local and systemic inflammation in AP does not require trypsinogen activation. NF-κB is activated early in acinar cells, independently of trypsinogen activation, and might be responsible for progression of AP.

Indexed as

Acinar CellsAnimalsCell DeathEnzyme ActivationInflammationIsoenzymesMiceMice, Inbred C57BLMice, KnockoutNF-kappa BPancreatitisTrypsinogenIsoenzymesNF-kappa BTrypsinogen

Identifiers

PMID21875495
PMCPMC3587766
OpenAlexW2069366124

What OpenQuestion holds

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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 OpenQuestion graph.