Evidence map›Paper›PMID 25105302›Full record

ReviewMolecular medicine (Cambridge, Mass.)2014

Cell death and DAMPs in acute pancreatitis.

Rui Kang, Michael T Lotze, Herbert J Zeh, Timothy R Billiar, Daolin Tang

Open access · goldAbstract readReview
In one paragraph

Review in Molecular medicine (Cambridge, Mass.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
95citing papers in PubMed, 1 pooled it
7.6field-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

95 citing papers in PubMed, 1 synthesis or guideline pooled it, 165 citations in OpenAlex.

  1. Guideline
  2. Trial
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Personalizing treatment of pancreatitis-associated chronic pain: the need for an integrated omics approach.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Damage-associated molecular patterns and coagulation.British journal of haematology · 2026
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

35 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

5 authors at 2 institutions in 1 country.

Rui KangDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Michael T LotzeDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Herbert J ZehDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Timothy R BilliarDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
Daolin TangDepartment of Surgery, University of Pittsburgh, Pittsburgh, Pennsylvania, United States of America.
UPMC Hillman Cancer Center · USUniversity of Pittsburgh · US

Funding

VECTOR CORE FACILITYP30CA047904 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Jessie Nedrow · 1988 to 2026
$158.0M
Targeting HMGB1-mediated Autophagy in Cancer TherapyR01CA160417 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI TANG, DAOLIN · 2012 to 2023
$3.0M
Pancreatic Ductal Adenocarcinoma is a disease of constitutive autophagyR01CA181450 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LOTZE, MICHAEL T, ZEH, HERBERT J · 2014 to 2018
$1.6M
NCI NIH HHS P30 CA047904NCI NIH HHS P30CA047904NCI NIH HHS R01 CA160417NCI NIH HHS R01CA160417NCI NIH HHS R01 CA181450NCI NIH HHS R01CA181450
6 · The paper itself

Abstract

Cell death and inflammation are key pathologic responses of acute pancreatitis (AP), the leading cause of hospital admissions for gastrointestinal disorders. It is becoming increasingly clear that damage-associated molecular pattern molecules (DAMPs) play an important role in the pathogenesis of AP by linking local tissue damage to systemic inflammation syndrome. Endogenous DAMPs released from dead, dying or injured cells initiate and extend sterile inflammation via specific pattern recognition receptors. Inhibition of the release and activity of DAMPs (for example, high mobility group box 1, DNA, histones and adenosine triphosphate) provides significant protection against experimental AP. Moreover, increased serum levels of DAMPs in patients with AP correlate with disease severity. These findings provide novel insight into the mechanism, diagnosis and management of AP. DAMPs might be an attractive therapeutic target in AP.

Indexed as

Adenosine TriphosphateCell DeathDNAHistonesHMGB1 ProteinHumansPancreatitisReceptors, Pattern RecognitionSystemic Inflammatory Response SyndromeAdenosine TriphosphateDNAHistonesHMGB1 ProteinHMGB1 protein, humanReceptors, Pattern Recognition

Identifiers

PMID25105302
PMCPMC4277549
OpenAlexW2333070971

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.