ArticleDiabetologia2014
SMAD2 disruption in mouse pancreatic beta cells leads to islet hyperplasia and impaired insulin secretion due to the attenuation of ATP-sensitive K+ channel activity.
Article in Diabetologia, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 37 citations in OpenAlex.
- Axonal regeneration and hyperglycemia in wound healing: a review on the role of activin A, TNFRSF10B, and Synaptophysin.Molecular biology reports · 2026Review
- RNA-binding protein Rbm38 as a multifaceted post-transcriptional regulator in zebrafish pancreatic development.Journal of molecular cell biology · 2026Article
- Increased TGF-β/Activin-Smad2 signaling is associated with pancreatic β-cell dysfunction and glucose intolerance in gestational diabetes mellitus.Molecular metabolism · 2026Article
- Lipotoxicity Induces β-cell Small Extracellular Vesicle-Mediated β-cell Dysfunction in Male Mice.Endocrinology · 2025Article
- Review
- Review
- Smad3 deficiency improves islet-based therapy for diabetes and diabetic kidney injury by promoting β cell proliferationTheranostics · 2022Article
- β-cell Smad2 null mice have improved β-cell function and are protected from diet-induced hyperglycemia.The Journal of biological chemistry · 2021Article
- Tet2 Controls the Responses of β cells to Inflammation in Autoimmune Diabetes.Nature communications · 2021Article
- Article
- TGF-β Signaling in Pancreatic Islet β Cell Development and Function.Endocrinology · 2021Review
- Towards a Functional Cure for Diabetes Using Stem Cell-Derived Beta Cells: Are We There Yet?Cells · 2021Review
- Emerging routes to the generation of functional β-cells for diabetes mellitus cell therapy.Nature reviews. Endocrinology · 2020Review
- Gdf11 gene transfer prevents high fat diet-induced obesity and improves metabolic homeostasis in obese and STZ-induced diabetic mice.Journal of translational medicine · 2019Article
- Combined Inhibition of DYRK1A, SMAD, and Trithorax Pathways Synergizes to Induce Robust Replication in Adult Human Beta Cells.Cell metabolism · 2019Article
- Antagonistic interaction between Nodal and insulin modulates pancreatic β-cell proliferation and survival.Cell communication and signaling : CCS · 2018Article
- The Role of the TGFβ Receptor Signaling Pathway in Adult Beta Cell Proliferation.International journal of molecular sciences · 2018Review
- Smad proteins differentially regulate obesity-induced glucose and lipid abnormalities and inflammation via class-specific control of AMPK-related kinase MPK38/MELK activity.Cell death & disease · 2018Article
- Article
- Integration of ATAC-seq and RNA-seq identifies human alpha cell and beta cell signature genes.Molecular metabolism · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aims/hypothesisThe TGF-β superfamily of ligands provides important signals for the development of pancreas islets. However, it is not yet known whether the TGF-β family signalling pathway is required for essential islet functions in the adult pancreas.
methodsTo identify distinct roles for the downstream components of the canonical TGF-β signalling pathway, a Cre-loxP system was used to disrupt SMAD2, an intracellular transducer of TGF-β signals, in pancreatic beta cells (i.e. Smad2β knockout [KO] mice). The activity of ATP-sensitive K(+) channels (KATP channels) was recorded in mutant beta cells using patch-clamp techniques.
resultsThe Smad2βKO mice exhibited defective insulin secretion in response to glucose and overt diabetes. Interestingly, disruption of SMAD2 in beta cells was associated with a striking islet hyperplasia and increased pancreatic insulin content, together with defective glucose-responsive insulin secretion. The activity of KATP channels was decreased in mutant beta cells. CONCLUSIONS/
interpretationThese results suggest that in the adult pancreas, TGF-β signalling through SMAD2 is crucial for not only the determination of beta cell mass but also the maintenance of defining features of mature pancreatic beta cells, and that this involves modulation of KATP channel activity.
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