Evidence map›Paper›PMID 25383781›Full record

ArticlePloS one2014

Deletion of apoptosis signal-regulating kinase 1 (ASK1) protects pancreatic beta-cells from stress-induced death but not from glucose homeostasis alterations under pro-inflammatory conditions.

Emilie Pepin, Arisa Higa, Carole Schuster-Klein, Catherine Bernard, Thierry Sulpice, Beatrice Guardiola, Eric Chevet, Thierry Alquier

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

12 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Triglycerides, Glucose Metabolism, and Type 2 Diabetes.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Review
  5. Article
  6. Mechanisms of exercise for diabetic neuropathic pain.Frontiers in aging neuroscience · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Review
  12. 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

8 authors at 5 institutions in 2 countries.

Emilie PepinBetagenex Inc, Laval, QC, Canada, H7V5B7.
Arisa HigaInserm U1053, Team Endoplasmic Reticulum Stress and Cancer, Université de Bordeaux, Bordeaux, France, 33076.
Carole Schuster-KleinGroupe de Recherche Servier, Suresnes, France, 92284 Cedex.
Catherine BernardGroupe de Recherche Servier, Suresnes, France, 92284 Cedex.
Thierry SulpiceBetagenex Inc, Laval, QC, Canada, H7V5B7; Physiogenex SAS, Labège, France, 31670.
Beatrice GuardiolaGroupe de Recherche Servier, Suresnes, France, 92284 Cedex.
Eric ChevetInserm U1053, Team Endoplasmic Reticulum Stress and Cancer, Université de Bordeaux, Bordeaux, France, 33076.
Thierry AlquierMontreal Diabetes Research Center, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CRCHUM), and Departments of Medicine, Biochemistry and Cell Biology and Pathology, Université de Montréal, Montréal, QC, Canada, H3T 1J4.
Servier (France) · FRCentre Hospitalier de l’Université de Montréal · CAInserm · FRPhysiogenex (France) · FRUniversité de Bordeaux · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType 2 diabetes is characterized by pancreatic beta-cell dysfunction and is associated with low-grade inflammation. Recent observations suggest that apoptosis signal-regulating kinase 1 (ASK1) is involved in beta-cell death in response to different stressors. In this study, we tested whether ASK1 deficiency protects beta-cells from glucolipotoxic conditions and cytokines treatment or from glucose homeostasis alteration induced by endotoxemia. METHODOLOGY/PRINCIPAL

findingsInsulin secretion was neither affected upon shRNA-mediated downregulation of ASK1 in MIN6 cells nor in islets from ASK1-deficient mice. ASK1 silencing in MIN6 cells and deletion in islets did not prevent the deleterious effect of glucolipotoxic conditions or cytokines on insulin secretion. However, it protected MIN6 cells from death induced by ER stress or palmitate and islets from short term caspase activation in response to cytokines. Moreover, endotoxemia induced by LPS infusion increased insulin secretion during hyperglycemic clamps but the response was similar in wild-type and ASK1-deficient mice. Finally, insulin sensitivity in the presence of LPS was not affected by ASK1-deficiency. CONCLUSIONS/SIGNIFICANCE: Our study demonstrates that ASK1 is not involved in beta-cell function and dysfunction but controls stress-induced beta-cell death.

Indexed as

AnimalsCells, CulturedCytokinesDiabetes Mellitus, Type 2GlucoseHumansInflammationInsulinInsulin-Secreting CellsInsulin SecretionLipopolysaccharidesMAP Kinase Kinase Kinase 5MiceMice, KnockoutPalmitic AcidStress, PhysiologicalCytokinesGlucoseInsulinLipopolysaccharidesMap3k5 protein, mouseMAP Kinase Kinase Kinase 5Palmitic Acid

Identifiers

PMID25383781
PMCPMC4226582
OpenAlexW2100877880

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.