Evidence map›Paper›PMID 42160450›Full record

ArticleScience translational medicine2026

A mitochondrial ROS-dependent antiviral response promotes β cell resilience and is diminished in donors with type 1 diabetes.

Leslie E Wagner, Olha Melnyk, Alissa N Muncy, Abigail Turner, Bryce E Duffett, Charanya Muralidharan, Michelle M Martinez-Irizarry, Matthew C Arvin, Kara S Orr, Wenting Wu and 6 more

Abstract read
In one paragraph

Article in Science translational medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

16 authors.

Leslie E WagnerDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0001-7821-8809
Olha MelnykDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0001-9085-6299
Alissa N MuncyDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.
Abigail TurnerDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.
Bryce E DuffettDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0009-0003-3715-6033
Charanya MuralidharanDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0002-4909-7056
Michelle M Martinez-IrizarryDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0001-5995-9281
Matthew C ArvinDepartment of Pediatrics, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0002-1744-2142
Kara S OrrCenter for Diabetes and Metabolic Diseases, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0002-1321-8581
Wenting WuCenter for Diabetes and Metabolic Diseases, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0003-0982-771X
Elisabetta ManduchiDepartment of Genetics and Institute for Diabetes, Obesity and Metabolism, University of Pennsylvania, Philadelphia, PA, USA.ORCID 0000-0002-4110-3714
Estefania Quesada-MasachsDiabetes Research Institute and Department of Medicine, Department of Rheumatology, University of Miami, Miami, FL, USA.ORCID 0000-0001-6033-1176
Jon D PiganelliDepartment of Medicine, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0003-2699-9011
Klaus H KaestnerDepartment of Genetics and Institute for Diabetes, Obesity and Metabolism, University of Pennsylvania, Philadelphia, PA, USA.ORCID 0000-0002-1228-021X
Joseph T BrozinickEli Lilly and Company, Indianapolis, IN, USA.ORCID 0000-0002-7946-3432
Amelia K LinnemannDepartment of Biochemistry and Molecular Biology, Indiana University School of Medicine, Indianapolis, IN, USA.ORCID 0000-0001-7356-4876

Funding

The Human Pancreas Analysis Program for Type 2 DiabetesU01DK123594 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI Robert Babak Faryabi, KLAUS H KAESTNER · 2019 to 2026
$25.0M
Penn integrated Human Pancreas procurement and Analysis ProgramUC4DK112217 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI BETTS, MICHAEL R, FELDMAN, MICHAEL D · 2016 to 2020
$17.8M
Integrated Islet Distribution Program (U24) - 2021U24DK098085 · NIDDK · BECKMAN RESEARCH INSTITUTE/CITY OF HOPE · PI Carmella Evans-Molina, Joyce Carol Niland · 2021 to 2026
$17.8M
Translation CoreP30DK097512 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI Amelia K Linnemann · 2015 to 2026
$17.4M
Supplement to Integrated Program for Human Pancreas Procurement and AnalysisUC4DK112232 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ATKINSON, MARK A., POWERS, ALVIN C · 2016 to 2020
$8.4M
Human Pancreas Analysis Program-T2DU01DK123716 · NIDDK · VANDERBILT UNIVERSITY MEDICAL CENTER · PI ATKINSON, MARK A., BOTTINO, RITA · 2019 to 2024
$6.6M
Specificity, Phenotype and Function of Pancreatic CD8 T Cells in Human Type 1 DiabetesR01AI092453 · NIAID · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Estefania Quesada Masachs · 2011 to 2026
$5.7M
Autophagy/antioxidant response coupling in pancreatic beta-cell homeostasis regulationR01DK124380 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI LINNEMANN, AMELIA K · 2021 to 2025
$2.0M
Functional and molecular characterization of the human islet interferon alpha responseR03DK127766 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI LINNEMANN, AMELIA K · 2020 to 2021
$334k
Beta Cell Heterogeneity in the Interferon Alpha ResponseF31DK137567 · NIDDK · INDIANA UNIVERSITY INDIANAPOLIS · PI WAGNER, LESLIE ELAINE · 2023 to 2024
$97k
NIAID NIH HHS R01 AI092453NIDDK NIH HHS F31 DK137567NIDDK NIH HHS P30 DK097512NIDDK NIH HHS R01 DK124380NIDDK NIH HHS R03 DK127766NIDDK NIH HHS U01 DK123594NIDDK NIH HHS U01 DK123716NIDDK NIH HHS U24 DK098085NIDDK NIH HHS UC4 DK112217NIDDK NIH HHS UC4 DK112232
6 · The paper itself

Abstract

Type 1 diabetes (T1D) is a multifactorial disease driven by genetic and environmental factors, including, potentially, viral infection. However, the mechanisms linking infection-associated cytokines to human β cell loss are poorly understood. Here, we coupled in vivo and in vitro imaging with genetic analysis to investigate the impact of interferon α (IFN-α), a cytokine produced during the immune response to viral infection or detection of unedited endogenous double-stranded RNAs, on human β cell physiology. We identified a subset of human β cells that acutely produce reactive oxygen species (ROS) in response to IFN-α and were more prevalent in islets from donors with lower body mass index and HbA1c. RNA sequencing of flow-sorted ROS

Indexed as

Antiviral AgentsDiabetes Mellitus, Type 1Insulin-Secreting CellsMitochondriaReactive Oxygen SpeciesTissue DonorsFemaleHumansInterferon-alphaMaleAntiviral AgentsInterferon-alphaReactive Oxygen Species

Identifiers

PMID42160450
PMCPMC13488389

What OpenQuestion 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 OpenQuestion graph.