ArticleJCI insight2022
Notch-mediated Ephrin signaling disrupts islet architecture and β cell function.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Genome-wide cell type-specific and sex-specific transcriptional dysregulation in the islet of Langerhans underlies islet dysfunction in Down syndrome-related diabetes.bioRxiv : the preprint server for biology · 2026Article
- Unraveling A-β+ ketosis-prone diabetes: An evolving diagnosis with an elusive pathogenesis.Journal of diabetes investigation · 2026Review
- In vivo functional profiling and structural characterization of the humanScience advances · 2026Article
- EFNA5 as an Oocyte-Derived Factor Enhances Developmental Competence by Modulating Oxidative Stress, Inflammation, and Apoptosis During In Vitro Maturation.Antioxidants (Basel, Switzerland) · 2025Article
- Type 2 diabetes mellitus in adults: pathogenesis, prevention and therapy.Signal transduction and targeted therapy · 2024 · on this mapReview
- Inhibition of Ephrin B2 Reverse Signaling Abolishes Multiple Myeloma Pathogenesis.Cancer research · 2024Article
- Advances and current concepts on Eph receptors and ephrins in upper digestive tract cancers.Frontiers in oncology · 2024Review
- The EPH/Ephrin System in Pancreatic Ductal Adenocarcinoma (PDAC): From Pathogenesis to Treatment.International journal of molecular sciences · 2023Review
- Axon Guidance Molecules in the Islets of Langerhans.Frontiers in endocrinology · 2022Review
- Data assimilation on mechanistic models of glucose metabolism predicts glycemic states in adolescents following bariatric surgery.Frontiers in physiology · 2022Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Altered islet architecture is associated with β cell dysfunction and type 2 diabetes (T2D) progression, but molecular effectors of islet spatial organization remain mostly unknown. Although Notch signaling is known to regulate pancreatic development, we observed "reactivated" β cell Notch activity in obese mouse models. To test the repercussions and reversibility of Notch effects, we generated doxycycline-dependent, β cell-specific Notch gain-of-function mice. As predicted, we found that Notch activation in postnatal β cells impaired glucose-stimulated insulin secretion and glucose intolerance, but we observed a surprising remnant glucose intolerance after doxycycline withdrawal and cessation of Notch activity, associated with a marked disruption of normal islet architecture. Transcriptomic screening of Notch-active islets revealed increased Ephrin signaling. Commensurately, exposure to Ephrin ligands increased β cell repulsion and impaired murine and human pseudoislet formation. Consistent with our mouse data, Notch and Ephrin signaling were increased in metabolically inflexible β cells in patients with T2D. These studies suggest that β cell Notch/Ephrin signaling can permanently alter islet architecture during a morphogenetic window in early life.
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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.