ArticleCommunications biology2020
Topologically selective islet vulnerability and self-sustained downregulation of markers for β-cell maturity in streptozotocin-induced diabetes.
Article in Communications biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- Discovery and validation of islet regenerative proteins secreted by human multipotent stromal cells.Stem cells translational medicine · 2026Article
- LDHA induces beta cell dedifferentiation in diabetes through metabolic and epigenetic reprogramming.Diabetologia · 2026Article
- Small things matter: Lack of extraislet β cells in type 1 diabetes.Science advances · 2025Article
- Small extracellular vesicles produced from canine adipose-derived mesenchymal stem cells mitigate diabetes mellitus in streptozotocin-induced mice via β-cell revitalization.BMC veterinary research · 2025Article
- Multiple low dose streptozotocin-induced diabetes as a model for studying autoimmune diabetes in humans.Animal models and experimental medicine · 2025Review
- Placenta-Derived Mesenchymal Stem Cells (pMSCs) Reverse Diabetes-Associated Endothelial Complications in a Preclinical Animal Model.International journal of molecular sciences · 2025Article
- Establishing a Dual Murine Model to Explore the Interactions Between Diabetes and Periodontitis in Mice.International journal of molecular sciences · 2025Article
- A pathophysiological intersection between metabolic biomarkers and memory: a longitudinal study in the STZ-induced diabetic mouse model.Frontiers in physiology · 2025Article
- Anti-diabetic effects of Dachaihu decoction combined withFrontiers in cell and developmental biology · 2025Article
- Interpreting single-cell and spatial omics data using deep neural network training dynamics.Nature computational science · 2024Article
- Targeting β-Cell Plasticity: A Promising Approach for Diabetes Treatment.Current issues in molecular biology · 2024Review
- Illuminating the complete ß-cell mass of the human pancreas- signifying a new view on the islets of Langerhans.Nature communications · 2024Article
- Geometric and topological characterization of the cytoarchitecture of islets of Langerhans.PLoS computational biology · 2023Article
- The Synergistic Influence of Polyflavonoids fromPharmaceutics · 2023Article
- Dose-dependent progression of multiple low-dose streptozotocin-induced diabetes in mice.Physiological genomics · 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
- Dose-dependent progression of multiple low dose streptozotocin-induced diabetes in mice.bioRxiv : the preprint server for biology · 2023Article
- Sex-dependent effects of canagliflozin and dapagliflozin on hemostasis in normoglycemic and hyperglycemic mice.Scientific reports · 2023Article
- Quantitative 3D OPT and LSFM datasets of pancreata from mice with streptozotocin-induced diabetes.Scientific data · 2022Article
- Guidelines on models of diabetic heart disease.American journal of physiology. Heart and circulatory physiology · 2022Review
Corrections and comments
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Authors and funding
15 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mouse models of Streptozotocin (STZ) induced diabetes represent the most widely used preclinical diabetes research systems. We applied state of the art optical imaging schemes, spanning from single islet resolution to the whole organ, providing a first longitudinal, 3D-spatial and quantitative account of β-cell mass (BCM) dynamics and islet longevity in STZ-treated mice. We demonstrate that STZ-induced β-cell destruction predominantly affects large islets in the pancreatic core. Further, we show that hyperglycemic STZ-treated mice still harbor a large pool of remaining β-cells but display pancreas-wide downregulation of glucose transporter type 2 (GLUT2). Islet gene expression studies confirmed this downregulation and revealed impaired β-cell maturity. Reversing hyperglycemia by islet transplantation partially restored the expression of markers for islet function, but not BCM. Jointly our results indicate that STZ-induced hyperglycemia results from β-cell dysfunction rather than β-cell ablation and that hyperglycemia in itself sustains a negative feedback loop restraining islet function recovery.
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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.