Evidence map›Paper›PMID 28536777›Full record

ReviewDigestive diseases and sciences2017

Genetic Risk in Chronic Pancreatitis: The Trypsin-Dependent Pathway.

Eszter Hegyi, Miklós Sahin-Tóth

Open access · hybridAbstract readReview
In one paragraph

Review in Digestive diseases and sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 7 pooled it
16.6field-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

112 citing papers in PubMed, 7 syntheses or guidelines pooled it, 192 citations in OpenAlex.

  1. Pooled it
  2. Risk of chronic pancreatitis in carriers of the c.180C>T (p.Gly60=) CTRC variant: case-control studies and meta-analysis.Pancreatology : official journal of the International Association of Pancreatology (IAP) ... [et al.] · 2023
    Pooled it
  3. Pooled it
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  7. Role of the CommonGenes · 2020
    Pooled it
  8. 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
  9. Article
  10. Reevaluating the role of TRPV6 deficiency in human and mouse pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Article
  11. Article
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  14. Article
  15. Pathologically relevant trypsinogen activation in pancreatitis.American journal of physiology. Gastrointestinal and liver physiology · 2026
    Review
  16. Review
  17. Article
  18. Article
  19. Review
  20. Article

52 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

2 authors at 1 institution in 1 country.

Eszter HegyiCenter for Exocrine Disorders, Department of Molecular and Cell Biology, Boston University Henry M. Goldman School of Dental Medicine, 72 East Concord Street, Evans-433, Boston, MA, 02118, USA.ORCID 0000-0002-9137-7561
Miklós Sahin-TóthCenter for Exocrine Disorders, Department of Molecular and Cell Biology, Boston University Henry M. Goldman School of Dental Medicine, 72 East Concord Street, Evans-433, Boston, MA, 02118, USA. miklos@bu.edu.ORCID 0000-0003-4513-9922
Boston University · US

Funding

Chymotrypsin in pancreatitisR01DK082412 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAHIN-TOTH, MIKLOS · 2009 to 2024
$5.8M
Molecular Pathomechanism of Hereditary PancreatitisR01DK058088 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SAHIN-TOTH, MIKLOS · 2001 to 2019
$5.3M
Pancreatic elastasesR01DK095753 · NIDDK · BOSTON UNIVERSITY MEDICAL CAMPUS · PI SAHIN-TOTH, MIKLOS · 2013 to 2016
$1.4M
NIDDK NIH HHS R01 DK058088NIDDK NIH HHS R01 DK082412NIDDK NIH HHS R01 DK095753
6 · The paper itself

Abstract

Genetic investigations have provided unique insight into the mechanism of chronic pancreatitis in humans and firmly established that uncontrolled trypsin activity is a central pathogenic factor. Mutations in the PRSS1, SPINK1, and CTRC genes promote increased activation of trypsinogen to trypsin by stimulation of autoactivation or by impairing protective trypsinogen degradation and/or trypsin inhibition. Here we review key genetic and biochemical features of the trypsin-dependent pathological pathway in chronic pancreatitis.

Indexed as

Genetic Predisposition to DiseaseGene Expression RegulationHumansMutationPancreatitis, ChronicTrypsinTrypsinChymotrypsinDigestive enzymesPancreasPancreatitisTrypsin inhibitorTrypsinogen activation

Identifiers

PMID28536777
PMCPMC5487703
OpenAlexW2617895952

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.