Evidence map›Paper›PMID 38918575›Full record

ArticleScientific reports2024

Molecular profiling of NOD mouse islets reveals a novel regulator of insulitis onset.

Andreas Frøslev Mathisen, Andrei Mircea Vacaru, Lucas Unger, Elena Mirela Lamba, Oana-Ana-Maria Mardare, Laura Maria Daian, Luiza Ghila, Ana-Maria Vacaru, Simona Chera

Abstract read
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
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

6 citing papers in PubMed.

  1. Article
  2. Review
  3. Experimental models in diabetes research.Laboratory animal research · 2026
    Review
  4. Review
  5. Article
  6. Lessons from a model: early glucagon dysfunction in type 2 diabetes.Pflugers Archiv : European journal of physiology · 2025
    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

9 authors.

Andreas Frøslev Mathisen *Department of Clinical Science, Mohn Research Center for Diabetes Precision Medicine, University of Bergen, Bergen, Norway.
Andrei Mircea Vacaru *BetaUpreg Research Group, Institute of Cellular Biology and Pathology "Nicolae Simionescu", Bucharest, Romania.
Lucas UngerDepartment of Clinical Science, Mohn Research Center for Diabetes Precision Medicine, University of Bergen, Bergen, Norway.
Elena Mirela LambaBetaUpreg Research Group, Institute of Cellular Biology and Pathology "Nicolae Simionescu", Bucharest, Romania.
Oana-Ana-Maria MardareBetaUpreg Research Group, Institute of Cellular Biology and Pathology "Nicolae Simionescu", Bucharest, Romania.
Laura Maria DaianBetaUpreg Research Group, Institute of Cellular Biology and Pathology "Nicolae Simionescu", Bucharest, Romania.
Luiza GhilaDepartment of Clinical Science, Mohn Research Center for Diabetes Precision Medicine, University of Bergen, Bergen, Norway.
Ana-Maria VacaruBetaUpreg Research Group, Institute of Cellular Biology and Pathology "Nicolae Simionescu", Bucharest, Romania. Ana.Vacaru@icbp.ro.
Simona CheraDepartment of Clinical Science, Mohn Research Center for Diabetes Precision Medicine, University of Bergen, Bergen, Norway. Simona.Chera@uib.no.

Funding

NO Grants 2014-2021 RO-NO-2019-0544Norges Forskningsråd 304615Novo Nordisk Fonden NNF21OC0067325
6 · The paper itself

Abstract

Non-obese diabetes (NOD) mice are an established, spontaneous model of type 1 diabetes in which diabetes develops through insulitis. Using next-generation sequencing, coupled with pathway analysis, the molecular fingerprint of early insulitis was mapped in a cohort of mice ranging from 4 to 12 weeks of age. The resulting dynamic timeline revealed an initial decrease in proliferative capacity followed by the emergence of an inflammatory signature between 6 and 8 weeks that increased to a regulatory plateau between 10 and 12 weeks. The inflammatory signature is identified by the activation of central immunogenic factors such as Infg, Il1b, and Tnfa, and activation of canonical inflammatory signaling. Analysis of the regulatory landscape revealed the transcription factor Atf3 as a potential novel modulator of inflammatory signaling in the NOD islets. Furthermore, the Hedgehog signaling pathway correlated with Atf3 regulation, suggesting that the two play a role in regulating islet inflammation; however, further studies are needed to establish the nature of this connection.

Indexed as

Activating Transcription Factor 3Diabetes Mellitus, Type 1Islets of LangerhansMice, Inbred NODSignal TransductionAnimalsDisease Models, AnimalFemaleGene Expression ProfilingHedgehog ProteinsInflammationMiceActivating Transcription Factor 3Atf3 protein, mouseHedgehog Proteins

Identifiers

PMID38918575
PMCPMC11199597

What Socratic holds

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Registered trials

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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 Socratic graph.