Evidence map›Paper›PMID 30660731›Full record

ReviewGastroenterology2019

Genetics, Cell Biology, and Pathophysiology of Pancreatitis.

Julia Mayerle, Matthias Sendler, Eszter Hegyi, Georg Beyer, Markus M Lerch, Miklós Sahin-Tóth

Open access · greenAbstract readReview
In one paragraph

Review in Gastroenterology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 203 papers, 11 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
203citing papers in PubMed, 11 pooled it
31.6field-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

203 citing papers in PubMed, 11 syntheses or guidelines pooled it, 359 citations in OpenAlex.

  1. Guideline
  2. Pooled it
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  10. Role of the CommonGenes · 2020
    Pooled it
  11. Pooled it
  12. Trial
  13. Assessing the burden and trends of pancreatitis in India from 1990-2021: An analysis of the global burden of disease database.Indian journal of gastroenterology : official journal of the Indian Society of Gastroenterology · 2026
    Article
  14. Article
  15. Genetic and pharmacologic modulations elucidate NRF2 protective role in acute pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

143 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

6 authors at 4 institutions in 3 countries.

Julia MayerleMedical Department II, University Hospital, LMU, Munich, Germany; Department of Medicine A, University Medicine Greifswald, Greifswald, Germany.
Matthias SendlerDepartment of Medicine A, University Medicine Greifswald, Greifswald, Germany.
Eszter HegyiInstitute for Translational Medicine, University of Pécs, Pécs, Hungary.
Georg BeyerMedical Department II, University Hospital, LMU, Munich, Germany.
Markus M LerchDepartment of Medicine A, University Medicine Greifswald, Greifswald, Germany. Electronic address: lerch@uni-greifswald.de.
Miklós Sahin-TóthCenter for Exocrine Disorders, Department of Molecular and Cell Biology, Boston University Henry M. Goldman School of Dental Medicine, Boston, Massachusetts.
Universitätsmedizin Greifswald · DEBoston University · USLMU Klinikum · DEUniversity of Pecs · HU

Funding

Molecular Pathomechanism of Hereditary PancreatitisR01DK058088 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAHIN-TOTH, MIKLOS · 2001 to 2019
$5.3M
Trypsin-dependent mechanisms in pancreatitisR01DK117809 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAHIN-TOTH, MIKLOS · 2018 to 2022
$2.5M
NIDDK NIH HHS R01 DK058088NIDDK NIH HHS R01 DK117809
6 · The paper itself

Abstract

Since the discovery of the first trypsinogen mutation in families with hereditary pancreatitis, pancreatic genetics has made rapid progress. The identification of mutations in genes involved in the digestive protease-antiprotease pathway has lent additional support to the notion that pancreatitis is a disease of autodigestion. Clinical and experimental observations have provided compelling evidence that premature intrapancreatic activation of digestive proteases is critical in pancreatitis onset. However, disease course and severity are mostly governed by inflammatory cells that drive local and systemic immune responses. In this article, we review the genetics, cell biology, and immunology of pancreatitis with a focus on protease activation pathways and other early events.

Indexed as

PancreasPancreatitisAnimalsApoptosisEnzyme ActivationGenetic Predisposition to DiseaseHumansInflammation MediatorsMutationNecrosisPeptide HydrolasesPhenotypePrognosisProtein FoldingRisk FactorsSignal TransductionInflammation MediatorsPeptide HydrolasesCell DeathGeneticsInflammationPancreatitisTrypsinogen

Identifiers

PMID30660731
PMCPMC6903413
OpenAlexW2910053234

What Socratic holds

Textmetadata
LicenceTDM
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.