Evidence map›Paper›PMID 26628584›Full record

ReviewEuropean journal of endocrinology2016

MECHANISMS IN ENDOCRINOLOGY: Alternative splicing: the new frontier in diabetes research.

Jonàs Juan-Mateu, Olatz Villate, Décio L Eizirik

Open access · greenAbstract readReview
In one paragraph

Review in European journal of endocrinology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
7.5field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 61 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. mRNA Isoforms and Variants in Health and Disease.International journal of molecular sciences · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Acute severe hypoglycemia alters mouse brain microvascular proteome.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2024
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. The missing heritability in type 1 diabetes.Diabetes, obesity & metabolism · 2022
    Review
  17. Article
  18. Review
  19. Enriched Alternative Splicing in Islets of Diabetes-Susceptible Mice.International journal of molecular sciences · 2021
    Article
  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

3 authors at 1 institution in 1 country.

Jonàs Juan-MateuMedical FacultyULB Center for Diabetes Research and Welbio, Université Libre de Bruxelles (ULB), Route de Lennik, 808 - CP618, B-1070 Brussels, Belgium deizirik@ulb.ac.be mjuanmat@ulb.ac.be.
Olatz VillateMedical FacultyULB Center for Diabetes Research and Welbio, Université Libre de Bruxelles (ULB), Route de Lennik, 808 - CP618, B-1070 Brussels, Belgium.
Décio L EizirikMedical FacultyULB Center for Diabetes Research and Welbio, Université Libre de Bruxelles (ULB), Route de Lennik, 808 - CP618, B-1070 Brussels, Belgium deizirik@ulb.ac.be mjuanmat@ulb.ac.be.
Université Libre de Bruxelles · BE

Funding

Biomarkers Of Beta Cell Stress In Type 1 Diabetes (BetaMarker)UC4DK104166 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI EIZIRIK, DECIO LAKS, EVANS-MOLINA, CARMELLA · 2014 to 2014
$2.4M
NIDDK NIH HHS UC4 DK104166
6 · The paper itself

Abstract

Type 1 diabetes (T1D) is a chronic autoimmune disease in which pancreatic β cells are killed by infiltrating immune cells and by cytokines released by these cells. This takes place in the context of a dysregulated dialogue between invading immune cells and target β cells, but the intracellular signals that decide β cell fate remain to be clarified. Alternative splicing (AS) is a complex post-transcriptional regulatory mechanism affecting gene expression. It regulates the inclusion/exclusion of exons into mature mRNAs, allowing individual genes to produce multiple protein isoforms that expand the proteome diversity. Functionally related transcript populations are co-ordinately spliced by master splicing factors, defining regulatory networks that allow cells to rapidly adapt their transcriptome in response to intra and extracellular cues. There is a growing interest in the role of AS in autoimmune diseases, but little is known regarding its role in T1D. In this review, we discuss recent findings suggesting that splicing events occurring in both immune and pancreatic β cells contribute to the pathogenesis of T1D. Splicing switches in T cells and in lymph node stromal cells are involved in the modulation of the immune response against β cells, while β cells exposed to pro-inflammatory cytokines activate complex splicing networks that modulate β cell viability, expression of neoantigens and susceptibility to immune-induced stress. Unveiling the role of AS in β cell functional loss and death will increase our understanding of T1D pathogenesis and may open new avenues for disease prevention and therapy.

Indexed as

Alternative SplicingDiabetes Mellitus, Type 1B-LymphocytesHumansInsulin-Secreting Cells

Identifiers

PMID26628584
PMCPMC5331159
OpenAlexW2190307541

What OpenQuestion holds

Textmetadata
LicenceTDM
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.