Evidence mapPaperPMID 42413288Full record

ArticleEBioMedicine2026

Transcriptomics of type 1 diabetes progression: a validation study in newly diagnosed patients.

Tomi Suomi, Inna Starskaia, Omid Rasool, Ubaid Ullah Kalim, Sylvaine Bruggraber, M Loredana Marcovecchio, Emile Hendricks, Lut Overbergh, Mark Peakman, Timothy Tree and 7 more

Abstract read
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Article in EBioMedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

17 authors.

Tomi SuomiTurku Bioscience Centre, University of Turku and Åbo Akademi University, FI-20520, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland.
Inna StarskaiaTurku Bioscience Centre, University of Turku and Åbo Akademi University, FI-20520, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland.
Omid RasoolTurku Bioscience Centre, University of Turku and Åbo Akademi University, FI-20520, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland.
Ubaid Ullah KalimTurku Bioscience Centre, University of Turku and Åbo Akademi University, FI-20520, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland.
Sylvaine BruggraberDepartment of Paediatrics, University of Cambridge, Cambridge, UK.
M Loredana MarcovecchioDepartment of Paediatrics, University of Cambridge, Cambridge, UK.
Emile HendricksDepartment of Paediatrics, University of Cambridge, Cambridge, UK.
Lut OverberghDepartment of Chronic Diseases and Metabolism, Endocrinology, Katholieke Universiteit Leuven, Leuven, Belgium.
Mark PeakmanImmunology & Inflammation Research Therapeutic Area, Sanofi, MA, USA; Department of Immunobiology, King's College, London, UK.
Timothy TreeDepartment of Immunobiology, King's College, London, UK.
Søren BrunakNovo Nordisk Foundation Center for Protein Research, Faculty of Health and Medical Sciences, University of Copenhagen, Copenhagen, Denmark.
Anke M SchulteSanofi-Aventis Deutschland GmbH, Frankfurt, Germany.
Chantal MathieuDepartment of Chronic Diseases and Metabolism, Endocrinology, Katholieke Universiteit Leuven, Leuven, Belgium.
Mikael KnipPaediatric Research Centre, University of Helsinki and Helsinki University Hospital, Helsinki, Finland; Research Program for Clinical and Molecular Metabolism, Faculty of Medicine, University of 9 Helsinki, Helsinki, Finland; Tampere Centre for Child Health Research, Tampere University Hospital, Tampere, Finland.
Riitta LahesmaaTurku Bioscience Centre, University of Turku and Åbo Akademi University, FI-20520, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland; Institute of Biomedicine, University of Turku, FI-20520, Turku, Finland. Electronic address: riitta.lahesmaa@utu.fi.
Laura L EloTurku Bioscience Centre, University of Turku and Åbo Akademi University, FI-20520, Turku, Finland; InFLAMES Research Flagship Center, University of Turku, Turku, Finland; Institute of Biomedicine, University of Turku, FI-20520, Turku, Finland. Electronic address: laura.elo@utu.fi.
INNODIA Consortium

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundType 1 diabetes is an autoimmune disease with significant long-term complications. Variability in the decline of insulin secretion after diagnosis complicates both the development of treatments and disease management. We previously reported that gene expression changes within the first year post-diagnosis were associated with C-peptide decline at two years in the first INNODIA cohort of patients with newly diagnosed type 1 diabetes. Here, we aimed to validate these findings in an independent follow-up cohort and to increase statistical power by combining the data from both cohorts.

methodsWe analysed transcriptomic data from a follow-up INNODIA cohort of 168 individuals with newly diagnosed type 1 diabetes to assess whether previously identified associations with disease progression could be replicated. We then combined data from the original and follow-up cohorts for integrated analysis. Longitudinal gene expression changes during the first year after diagnosis were examined in relation to disease progression, alongside age and estimated immune cell abundances.

findingsAnalysis of the follow-up cohort validated the previously observed longitudinal changes in gene expression during the first year after diagnosis. In the combined dataset, transcriptomic analysis identified a large number of genes that were differentially expressed during the first year after disease onset. More rapid disease progression was associated with younger age and a relative decrease in neutrophil abundance. In addition, changes in the expression of several genes were associated with the rate of disease progression.

interpretationThese findings support the existence of biological heterogeneity in disease progression after diagnosis of type 1 diabetes and contribute to an improved understanding of the molecular dynamics associated with disease progression. These findings may help future studies aiming to enable patient stratification and design of more targeted and personalised therapeutic approaches in type 1 diabetes.

fundingThis project has received funding from the Innovative Medicines Initiative 2 Joint Undertaking under grant agreement No 115797 (INNODIA) and No 945268 (INNODIA HARVEST).

Indexed as

Diabetes Mellitus, Type 1Gene Expression ProfilingTranscriptomeAdolescentAdultChildC-PeptideDisease ProgressionFemaleGene Expression RegulationHumansMaleYoung AdultC-PeptideBeta cell declineC-peptideDisease progressionTranscriptomicsType 1 diabetes

Identifiers

PMID42413288
PMCPMC13355739

What Socratic holds

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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.