ArticleDiabetes2020
HB-EGF Signaling Is Required for Glucose-Induced Pancreatic β-Cell Proliferation in Rats.
Article in Diabetes, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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
25 citing papers in PubMed, 31 citations in OpenAlex.
- ALIX-dependent small extracellular vesicles from tissue-resident mesenchymal cells regulate pancreatic β cell proliferation in obesity.Science advances · 2026Article
- Identification of Centrosome Duplication-Related Biomarkers in Hypertrophic Cardiomyopathy Through Integrative Multi-Omics, Single-Cell Transcriptomics, and Experimental Validation.Journal of the American Heart Association · 2026Article
- Single-Cell Maps Reveal Novel Mechanisms of Ferroptosis and Biomarkers in Diabetic Nephropathy.Current medicinal chemistry · 2026Article
- From mucus secretion to immune surveillance: the evolving roles of goblet cells in intestinal homeostasis and inflammation.Frontiers in immunology · 2026Review
- A review of epidermal growth factor receptor ligands in glucose homeostasis.Frontiers in endocrinology · 2026Review
- Epigen-mediated mechanisms to alleviate glucose homeostasis disruptions in diet-induced obese and STZ-induced diabetic mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Review
- MMP3 mediates E2-induced bovine endometrial cell proliferation by releasing HB-EGF.The Journal of reproduction and development · 2025Article
- Single-cell RNA sequencing identifies endothelial-derived HBEGF as promoting pancreatic beta cell proliferation in mice via the EGFR-Kmt5a-H4K20me pathway.Diabetologia · 2025Article
- Islet single-cell transcriptomic profiling during obesity-induced beta cell expansion in female mice.iScience · 2025Article
- EGF receptor in organ development, tissue homeostasis and regeneration.Journal of biomedical science · 2025Review
- Article
- Review
- Phogrin Regulates High-Fat Diet-Induced Compensatory Pancreatic β-Cell Growth by Switching Binding Partners.Nutrients · 2024Article
- A Supportive Role of Mesenchymal Stem Cells on Insulin-Producing Langerhans Islets with a Specific Emphasis on The Secretome.Biomedicines · 2023Review
- Membrane protease prostasin promotes insulin secretion by regulating the epidermal growth factor receptor pathway.Scientific reports · 2023Article
- Pancreatic loss of Mig6 alters murine endocrine cell fate and protects functional beta cell mass in an STZ-induced model of diabetes.bioRxiv : the preprint server for biology · 2023Article
- A single-cell human islet interactome atlas identifies disrupted autocrine and paracrine communications in type 2 diabetes.NAR genomics and bioinformatics · 2022Article
- Epigenetic and transcriptomic alterations in offspring born to women with type 1 diabetes (the EPICOM study).BMC medicine · 2022Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
The molecular mechanisms of β-cell compensation to metabolic stress are poorly understood. We previously observed that nutrient-induced β-cell proliferation in rats is dependent on epidermal growth factor receptor (EGFR) signaling. The aim of this study was to determine the role of the EGFR ligand heparin-binding EGF-like growth factor (HB-EGF) in the β-cell proliferative response to glucose, a β-cell mitogen and key regulator of β-cell mass in response to increased insulin demand. We show that exposure of isolated rat and human islets to HB-EGF stimulates β-cell proliferation. In rat islets, inhibition of EGFR or HB-EGF blocks the proliferative response not only to HB-EGF but also to glucose. Furthermore, knockdown of HB-EGF in rat islets blocks β-cell proliferation in response to glucose ex vivo and in vivo in transplanted glucose-infused rats. Mechanistically, we demonstrate that HB-EGF mRNA levels are increased in β-cells in response to glucose in a carbohydrate-response element-binding protein (ChREBP)-dependent manner. In addition, chromatin immunoprecipitation studies identified ChREBP binding sites in proximity to the HB-EGF gene. Finally, inhibition of Src family kinases, known to be involved in HB-EGF processing, abrogated glucose-induced β-cell proliferation. Our findings identify a novel glucose/HB-EGF/EGFR axis implicated in β-cell compensation to increased metabolic demand.
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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.