ArticleNature communications2025
Pancreatic β-cell regeneration in situ by the ALK3 agonist THR-123.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- 'Remarkably encouraging': stem-cell treatments for autoimmune diseases enter new phase.Nature · 2026Article
- Syntaxin-4, a key exocytosis mediating protein, shows heterogeneous expression in insulin-positive cells of human donors with new-onset and longer duration of type 1 diabetes: comparison with non-diabetic autoantibody-positive and -negative donors.Journal of molecular histology · 2026Article
- Pharmacological therapies for type 2 diabetes: future approaches.Diabetologia · 2026Review
- THR-123, a novel BMP-7 mimetic that activates Akt phosphorylation and inhibits cardiomyocyte apoptosis and inflammation, protects the heart from myocardial injury in a Rat model.Frontiers in cardiovascular medicine · 2026Article
- β-Cell Neogenesis From the Pancreatic Ductal Epithelium Revealed Dynamically by Long-term Intravital Imaging.Diabetes · 2025Article
- Efficient transduction of pancreas tissue slices with genetically encoded calcium integrators.bioRxiv : the preprint server for biology · 2025Article
- Recent Updates on Diabetes and Bone.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
20 authors.
Funding
Abstract
The demonstration that BMP signaling activates progenitor-like populations within pancreatic ducts supports the potential use of BMP receptor agonists to induce islet neogenesis in situ. In this context, we tested the ability of THR-123, a cyclic peptide with BMP-7-like activity, to regenerate β-cell mass in diabetic mice. We show here that treatment with THR-123 reduces hyperglycemia through the rapid formation of new BrdU-labeled islets, many in apposition to ducts. These islets, unlike those from non-diabetic controls, feature an extensive intrainsular network of ductal tissue. The earlier stages of THR-123-induced β-cell formation were reproduced in live pancreatic slices, an organotypic model that allowed us to visualize ductal cells transitioning to glucose-responsive insulin-expressing cells in real time. scRNAseq analyses further suggest that this transition occurs through a hybrid ducto-acinar stage similar to that previously reported in humans. Taken together, our data support the conclusion that these islets arise predominantly by neogenesis. These results pave the way for the design of pharmacological strategies to treat insulin-dependent diabetes.
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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.