ArticleDiabetes2017
SMAD3/Stat3 Signaling Mediates β-Cell Epithelial-Mesenchymal Transition in Chronic Pancreatitis-Related Diabetes.
Article in Diabetes, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Endoplasmic reticulum stress and forkhead box protein O1 inhibition mediate palmitic acid and high glucose-induced β-cell dedifferentiation.World journal of diabetes · 2025Article
- Targeting macrophages and ion homeostasis in T2D: new genes and therapeutic pathways identified.Frontiers in immunology · 2025Article
- TGF-β1 induces PD-1 expression in macrophages through SMAD3/STAT3 cooperative signaling in chronic inflammation.JCI insight · 2024Article
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- Editorial: Cystic fibrosis-related diabetes.Frontiers in endocrinology · 2024Article
- Article
- Bone-marrow derived cells do not contribute to new beta-cells in the inflamed pancreas.Frontiers in immunology · 2023Article
- Article
- Role of angiogenesis in beta-cell epithelial-mesenchymal transition in chronic pancreatitis-induced diabetes.Laboratory investigation; a journal of technical methods and pathology · 2022Article
- Deletion of Smooth Muscle Lethal Giant Larvae 1 Promotes Neointimal Hyperplasia in Mice.Frontiers in pharmacology · 2022Article
- Role of TGF-β in pancreatic ductal adenocarcinoma progression and PD-L1 expression.Cellular oncology (Dordrecht, Netherlands) · 2021Article
- Insulin-positive ductal cells do not migrate into preexisting islets during pregnancy.Experimental & molecular medicine · 2021Article
- Mechanisms of Post-Pancreatitis Diabetes Mellitus and Cystic Fibrosis-Related Diabetes: A Review of Preclinical Studies.Frontiers in endocrinology · 2021Review
- Tubular STAT3 Limits Renal Inflammation in Autosomal Dominant Polycystic Kidney Disease.Journal of the American Society of Nephrology : JASN · 2020Article
- Placental growth factor in beta cells plays an essential role in gestational beta-cell growth.BMJ open diabetes research & care · 2020Article
- STAT3 dictates β-cell apoptosis by modulating PTEN in streptozocin-induced hyperglycemia.Cell death and differentiation · 2020Article
- Pathological Mechanisms in Diabetes of the Exocrine Pancreas: What's Known and What's to Know.Frontiers in physiology · 2020Review
- Evidence of a developmental origin for β-cell heterogeneity using a dual lineage-tracing technology.Development (Cambridge, England) · 2019Article
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Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Many patients with chronic pancreatitis develop diabetes (chronic pancreatitis-related diabetes [CPRD]) through an undetermined mechanism. Here we used long-term partial pancreatic duct ligation (PDL) as a model to study CPRD. We found that long-term PDL induced significant β-cell dedifferentiation, followed by a time-dependent decrease in functional β-cell mass-all specifically in the ligated tail portion of the pancreas (PDL-tail). High levels of transforming growth factor β1 (TGFβ1) were detected in the PDL-tail and were mainly produced by M2 macrophages at the early stage and by activated myofibroblasts at the later stage. Loss of β-cell mass was then found to result from TGFβ1-triggered epithelial-mesenchymal transition (EMT) by β-cells, rather than resulting directly from β-cell apoptosis. Mechanistically, TGFβ1-treated β-cells activated expression of the EMT regulator gene Snail in a SMAD3/Stat3-dependent manner. Moreover, forced expression of forkhead box protein O1 (FoxO1), an antagonist for activated Stat3, specifically in β-cells ameliorated β-cell EMT and β-cell loss and prevented the onset of diabetes in mice undergoing PDL. Together, our data suggest that chronic pancreatitis may trigger TGFβ1-mediated β-cell EMT to lead to CPRD, which could substantially be prevented by sustained expression of FoxO1 in β-cells.
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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.