Evidence map›Paper›PMID 21577290›Full record

ArticleWorld journal of gastrointestinal pharmacology and therapeutics2010

Inflammatory role of the acinar cells during acute pancreatitis.

Isabel De Dios

Open access · hybridAbstract read
In one paragraph

Article in World journal of gastrointestinal pharmacology and therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 23% 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

14 citing papers in PubMed, 43 citations in OpenAlex.

  1. Genetic and pharmacologic modulations elucidate NRF2 protective role in acute pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Article
  2. Article
  3. Contextual AI models for single-cell protein biology.bioRxiv : the preprint server for biology · 2024
    Article
  4. Review
  5. Golimumab Ameliorates Pancreatic Inflammatory Response in the Cerulein-Induced Acute Pancreatitis in Rats.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2022
    Article
  6. Article
  7. Adenosine Kinase Inhibition Prevents Severe Acute PancreatitisFrontiers in cell and developmental biology · 2022
    Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Review
  13. Article
  14. 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

1 author at 1 institution in 1 country.

Isabel De DiosIsabel De Dios, Department of Physiology and Pharmacology, University of Salamanca, Salamanca 37007, Spain.
Universidad de Salamanca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pancreatic acinar cells are secretory cells whose main function is to synthesize, store and finally release digestive enzymes into the duodenum. However, in response to noxious stimuli, acinar cells behave like real inflammatory cells because of their ability to activate signalling transduction pathways involved in the expression of inflammatory mediators. Mediated by the kinase cascade, activation of Nuclear factor-κB, Activating factor-1 and Signal transducers and activators of transcription transcription factors has been demonstrated in acinar cells, resulting in overexpression of inflammatory genes. In turn, kinase activity is down-regulated by protein phosphatases and the final balance between kinase and phosphatase activity will determine the capability of the acinar cells to produce inflammatory factors. The kinase/phosphatase pair is a redox-sensitive system in which kinase activation overwhelms phosphatase activity under oxidant conditions. Thus, the oxidative stress developed within acinar cells at early stages of acute pancreatitis triggers the activation of signalling pathways involved in the up-regulation of cytokines, chemokines and adhesion molecules. In this way, acinar cells trigger the release of the first inflammatory signals which can mediate the activation and recruitment of circulating inflammatory cells into the injured pancreas. Accordingly, the role of acinar cells as promoters of the inflammatory response in acute pancreatitis may be considered. This concept leads to amplifying the focus from leukocyte to acinar cells themselves, to explain the local inflammation in early pancreatitis.

Indexed as

Acinar cellsAcute pancreatitisInflammatory mediatorsSignal pathways

Identifiers

PMID21577290
PMCPMC3091137
OpenAlexW2067582182

What OpenQuestion holds

Textmetadata
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.