Evidence map›Paper›PMID 33087696›Full record

ArticleCell death & disease2020

Impaired autophagy increases susceptibility to endotoxin-induced chronic pancreatitis.

L Xia, Z Xu, X Zhou, F Bergmann, N Grabe, M W Büchler, J P Neoptolemos, T Hackert, G Kroemer, F Fortunato

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
3.5field-weighted citation impact, top 7% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Pancreatic involvement inMolecular genetics and metabolism reports · 2025
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Autophagy and the pancreas: Healthy and disease states.Frontiers in cell and developmental biology · 2024
    Review
  11. Farnesoid X receptor activation inhibits pancreatic carcinogenesis.Biochimica et biophysica acta. Molecular basis of disease · 2023
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. 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

10 authors at 2 institutions in 5 countries.

L XiaDepartment of General, Visceral and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany.
Z XuDepartment of General, Visceral and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany.
X ZhouDepartment of General, Visceral and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany.
F BergmannInstitute of Pathology; University Hospital Heidelberg, Heidelberg, Germany.
N GrabeNational Center for Tumor Diseases (NCT), University Hospital Heidelberg, Heidelberg, Germany.
M W BüchlerDepartment of General, Visceral and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany.
J P NeoptolemosDepartment of General, Visceral and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany.ORCID 0000-0002-6201-7399
T HackertDepartment of General, Visceral and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany.
G KroemerEquipe labellisée par la Ligue contre le cancer, Université de Paris, Sorbonne Université, INSERM U1138, Centre de Recherche des Cordeliers, Paris, France. kroemer@orange.fr.
F FortunatoDepartment of General, Visceral and Transplantation Surgery, University Hospital Heidelberg, Heidelberg, Germany. Franco.Fortunato@uni-heidelberg.de.ORCID 0000-0002-6711-5828
Heidelberg University · DEKarolinska University Hospital · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic pancreatitis (CP) is associated with elevated plasma levels of bacterial lipopolysaccharide (LPS) and we have demonstrated reduced acinar cell autophagy in human CP tissue. Therefore, we investigated the role of autophagy in experimental endotoxin-induced pancreatic injury and aimed to identify LPS in human CP tissue. Pancreatic Atg7-deficient mice were injected with a single sub-lethal dose of LPS. Expression of autophagy, apoptosis, necroptosis, and inflammatory markers was determined 3 and 24 h later utilizing immunoblotting and immunofluorescence. The presence of LPS in pancreatic tissue from mice and from patients and healthy controls was determined using immunohistochemistry, immunoblots, and chromogenic assay. Mice lacking pancreatic autophagy exhibited local signs of inflammation and were particularly sensitive to the toxic effect of LPS injection as compared to control mice. In response to LPS, Atg7

Indexed as

Acinar CellsAnimalsAutophagyCeruletideEndotoxinsHumansInflammationLipopolysaccharidesMice, TransgenicPancreatitis, ChronicCeruletideEndotoxinsLipopolysaccharides

Identifiers

PMID33087696
PMCPMC7578033
OpenAlexW3093797316

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.