ArticleJCI insight2018
Virus-like infection induces human β cell dedifferentiation.
Article in JCI insight, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
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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.
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.
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Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.
- The power of TOPMed imputation for the discovery of Latino-enriched rare variants associated with type 2 diabetes.Diabetologia · 2023Pooled it
- Human β-Cell Dedifferentiation and Diabetes.Journal of diabetes · 2026Review
- SOX9: dosage- and context-dependent functions in pancreatic development and β-cell biology.Cell communication and signaling : CCS · 2026Review
- The Hippo terminal effector YAP boosts enterovirus replication in type 1 diabetes.Nature communications · 2025Article
- Loss of insulin-expressing extra-islet cells in type 1 diabetes is accompanied with increased number of glucagon-expressing extra-islet cells.Virchows Archiv : an international journal of pathology · 2025Article
- Targeting β-Cell Plasticity: A Promising Approach for Diabetes Treatment.Current issues in molecular biology · 2024Review
- Islet cell stress induced by insulin-degrading enzyme deficiency promotes regeneration and protection from autoimmune diabetes.iScience · 2024Article
- Loss of β-cell identity and dedifferentiation, not an irreversible process?Frontiers in endocrinology · 2024Review
- Beta cell dedifferentiation in type 1 diabetes: sacrificing function for survival?Frontiers in endocrinology · 2024Article
- ZBTB12 is a molecular barrier to dedifferentiation in human pluripotent stem cells.Nature communications · 2023Article
- Enteroviral infections are not associated with type 2 diabetes.Frontiers in endocrinology · 2023Article
- COVID-19 and diabetes in children.Annals of pediatric endocrinology & metabolism · 2022Article
- MafB MaintainsMolecular and cellular biology · 2022Article
- Characterization of the Secretome, Transcriptome, and Proteome of Human β Cell Line EndoC-βH1.Molecular & cellular proteomics : MCP · 2022Article
- Review
- SOX9 negatively regulates the RLR antiviral signaling by targeting MAVS.Virus genes · 2022Article
- Article
- The m6A methylation profiles of immune cells in type 1 diabetes mellitus.Frontiers in immunology · 2022Article
- Increased Expression of Viral Sensor MDA5 in Pancreatic Islets and in Hormone-Negative Endocrine Cells in Recent Onset Type 1 Diabetic Donors.Frontiers in immunology · 2022Article
- SARS-CoV-2 Infection and Pancreatic β Cell Failure.Biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes (T1D) is a chronic disease characterized by an autoimmune-mediated destruction of insulin-producing pancreatic β cells. Environmental factors such as viruses play an important role in the onset of T1D and interact with predisposing genes. Recent data suggest that viral infection of human islets leads to a decrease in insulin production rather than β cell death, suggesting loss of β cell identity. We undertook this study to examine whether viral infection could induce human β cell dedifferentiation. Using the functional human β cell line EndoC-βH1, we demonstrate that polyinosinic-polycytidylic acid (PolyI:C), a synthetic double-stranded RNA that mimics a byproduct of viral replication, induces a decrease in β cell-specific gene expression. In parallel with this loss, the expression of progenitor-like genes such as SOX9 was activated following PolyI:C treatment or enteroviral infection. SOX9 was induced by the NF-κB pathway and also in a paracrine non-cell-autonomous fashion through the secretion of IFN-α. Lastly, we identified SOX9 targets in human β cells as potentially new markers of dedifferentiation in T1D. These findings reveal that inflammatory signaling has clear implications in human β cell dedifferentiation.
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Registered trials
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.