Evidence map›Paper›PMID 15632003›Full record

ArticleThe American journal of pathology2005

Chronic alcohol consumption accelerates fibrosis in response to cerulein-induced pancreatitis in rats.

Xiaoying Deng, Lin Wang, Mary S Elm, David Gabazadeh, Greg J Diorio, Patricia K Eagon, David C Whitcomb

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
9.9field-weighted citation impact, top 2% 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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 132 citations in OpenAlex.

  1. Guideline
  2. CREB Fuels Tumorigenesis in Alcoholic Pancreatitis.Cellular and molecular gastroenterology and hepatology · 2026
    Article
  3. Acute pancreatitis experimental models, advantages and disadvantages.Journal of physiology and biochemistry · 2025
    Review
  4. Protein kinase D1 - A targetable mediator of pancreatic cancer development.Biochimica et biophysica acta. Molecular cell research · 2024
    Review
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  9. Article
  10. Review
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  17. Article
  18. Role of eosinophils in the initiation and progression of pancreatitis pathogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2018
    Article
  19. Review
  20. Review
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 3 institutions in 1 country.

Xiaoying DengDepartment of Medicine, University of Pittsburgh, Pittsburgh, PA 15213, USA.
Lin Wang
Mary S Elm
David Gabazadeh
Greg J Diorio
Patricia K Eagon
David C Whitcomb
University of Pittsburgh · USUniversity of Pittsburgh Medical Center · USVA Pittsburgh Healthcare System · US

Funding

NIAAA NIH HHS R01 AA10855
6 · The paper itself

Abstract

Alcohol consumption is a risk factor for chronic pancreatitis (CP), but the mechanism in humans remains obscure because prolonged alcohol consumption in most humans and animal models fails to produce alcoholic chronic pancreatitis (ACP). We hypothesize that the process leading to ACP is triggered by a sentinel acute pancreatitis (AP) event; this event causes recruitment of inflammatory cells, which initiates fibrosis driven by the anti-inflammatory response to recurrent AP and/or chronic oxidative stress. The aim was to determine whether chronic alcohol consumption accelerates fibrosis in response to cerulein-induced pancreatitis in the rat. Wistar male rats were pair-fed control (C) or 5% ethanol (E) Lieber-DeCarli liquid diets. Animals were studied without pancreatitis (P0), with cerulein pancreatitis induced once (P1), or with cerulein-induced pancreatitis weekly for 3 weeks (P3). AP markers, inflammation, and fibrosis were measured histologically, by gene expression profiling and protein expression. Macrophage infiltration was reduced in EP0 versus CP0 rats, but the pattern was reversed after AP. Microabscess, severe necrosis, and early calcification were only induced in the EP3 rats. Fibrosis was significantly induced in the EP3 rats versus EP1, CP1, and CP3 by histology, hydroxyproline content, and mRNA expression for collagen alpha1(1) and procollagen alpha2(1). Proinflammatory cytokine mRNAs were up-regulated shortly after induction of AP, while the anti-inflammatory cytokines (interleukin-10 and transforming growth factor-beta) were strongly up-regulated later and in parallel with fibrogenesis, especially in the EP3 rats. Pancreatic fibrosis develops after repeated episodes of AP and is potentiated by alcohol. Expression of fibrosis-associated genes was associated with expression of anti-inflammatory cytokines in alcohol-fed rats.

Indexed as

Alcohol DrinkingAlcoholismAnimalsCeruletideChronic DiseaseDisease Models, AnimalDNA PrimersFibrosisGene Expression RegulationMalePancreatitisPolymerase Chain ReactionRatsRats, WistarRNA, MessengerCeruletideDNA PrimersRNA, Messenger

Identifiers

PMID15632003
PMCPMC1602301
OpenAlexW2079877716

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.