Evidence map›Paper›PMID 22586407›Full record

ArticleFrontiers in physiology2012

Role of Intrapancreatic SPINK1/Spink3 Expression in the Development of Pancreatitis.

Masaki Ohmuraya, Aki Sugano, Masahiko Hirota, Yutaka Takaoka, Ken-Ichi Yamamura

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 36 citations in OpenAlex.

  1. Review
  2. ECRG2/SPINK7 Tumor Suppressor as Modulator of DNA Damage Response.International journal of molecular sciences · 2024
    Review
  3. Autophagy and the pancreas: Healthy and disease states.Frontiers in cell and developmental biology · 2024
    Review
  4. Article
  5. Review
  6. Functional Roles of SPINK1 in Cancers.International journal of molecular sciences · 2021
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Cell death and DAMPs in acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2014
    Review
  14. Article
  15. Article
  16. Recent advances in pancreatology.Frontiers in physiology · 2014
    Article
  17. Article
  18. Article
  19. New insights into the pathogenesis of pancreatitis.Current opinion in gastroenterology · 2013
    Review
  20. 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

5 authors at 3 institutions in 1 country.

Masaki OhmurayaInstitute of Resource Development and Analysis, Kumamoto University Kumamoto, Japan.
Aki Sugano
Masahiko Hirota
Yutaka Takaoka
Ken-Ichi Yamamura
Kobe University · JPKumamoto University · JPKumamoto Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Studies on hereditary pancreatitis have provided evidence in favor of central role for trypsin activity in the disease. Identification of genetic variants of trypsinogen linked the protease to the onset of pancreatitis, and biochemical characterization proposed an enzymatic gain of function as the initiating mechanism. Mutations of serine protease inhibitor Kazal type 1 gene (SPINK1) are shown to be associated with hereditary pancreatitis. We previously reported that Spink3 (a mouse homolog gene of human SPINK1) deficient mice showed excessive autophagy, followed by inappropriate trypsinogen activation in the exocrine pancreas. These data indicate that the role of SPINK1/Spink3 is not only trypsin inhibitor, but also negative regulator of autophagy. On the other hand, recent studies showed that high levels of SPINK1 protein detected in a serum or urine were associated with adverse outcome in various cancer types. It has been suggested that expression of SPINK1 and trypsin is balanced in normal tissue, but this balance could be disrupted during tumor progression. Based on the structural similarity between SPINK1 and epidermal growth factor (EGF), we showed that SPINK1 protein binds and activates EGF receptor, thus acting as a growth factor on tumor cell lines. In this review, we summarize the old and new roles of SPINK1/Spink3 in trypsin inhibition, autophagy, and cancer cell growth. These new functions of SPINK1/Spink3 may be related to the development of chronic pancreatitis.

Indexed as

autophagychronic pancreatitisEGFEGFRhereditary pancreatitisSPINK1Spink3trypsinogen

Identifiers

PMID22586407
PMCPMC3345944
OpenAlexW2098346462

What OpenQuestion holds

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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.