ArticleDiabetes2014
A smad signaling network regulates islet cell proliferation.
Article in Diabetes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 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
51 citing papers in PubMed, 77 citations in OpenAlex.
- Increased TGF-β/Activin-Smad2 signaling is associated with pancreatic β-cell dysfunction and glucose intolerance in gestational diabetes mellitus.Molecular metabolism · 2026Article
- The central role of IL-6 in the differential effects of GLP-1 receptor agonists and metformin across multiple health conditions.Frontiers in immunology · 2026Review
- Pancreatic β-cell regeneration in situ by the ALK3 agonist THR-123.Nature communications · 2025Article
- Mechanistic insights and approaches for beta cell regeneration.Nature chemical biology · 2025Review
- A Two-Sample Mendelian Randomization Study of Basophil Count and Risk of Gestational Diabetes Mellitus.International journal of women's health · 2025Article
- TGF-β, IL-1β, IL-6 levels and TGF-β/Smad pathway reactivity regulate the link between allergic diseases, cancer risk, and metabolic dysregulations.Frontiers in immunology · 2024Article
- Regeneration of Pancreatic Beta Cells by Modulation of Molecular Targets Using Plant-Derived Compounds: Pharmacological Mechanisms and Clinical Potential.Current issues in molecular biology · 2023Review
- Review
- Accelerated Generation of Extra-Islet Insulin-Producing Cells in Diabetic Rats, Treated with Sodium Phthalhydrazide.International journal of molecular sciences · 2022Article
- Review
- AANG Prevents Smad3-dependent Diabetic Nephropathy by Restoring Pancreatic β-Cell Development in db/db Mice.International journal of biological sciences · 2022Article
- 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
- Smad3 deficiency promotes beta cell proliferation and function inTheranostics · 2021Article
- Human Beta Cell Regenerative Drug Therapy for Diabetes: Past Achievements and Future Challenges.Frontiers in endocrinology · 2021Review
- Key regulatory genes and signaling pathways involved in islet culture: a bioinformatic analysis.International journal of clinical and experimental pathology · 2021Article
- Good Cop, Bad Cop: The Opposing Effects of Macrophage Activation State on Maintaining or Damaging Functional β-Cell Mass.Metabolites · 2020Review
- SMAD7 enhances adult β-cell proliferation without significantly affecting β-cell function in mice.The Journal of biological chemistry · 2020Article
- Protection from β-cell apoptosis by inhibition of TGF-β/Smad3 signaling.Cell death & disease · 2020Article
- Evidence of a developmental origin for β-cell heterogeneity using a dual lineage-tracing technology.Development (Cambridge, England) · 2019Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
Abstract
Pancreatic β-cell loss and dysfunction are critical components of all types of diabetes. Human and rodent β-cells are able to proliferate, and this proliferation is an important defense against the evolution and progression of diabetes. Transforming growth factor-β (TGF-β) signaling has been shown to affect β-cell development, proliferation, and function, but β-cell proliferation is thought to be the only source of new β-cells in the adult. Recently, β-cell dedifferentiation has been shown to be an important contributory mechanism to β-cell failure. In this study, we tie together these two pathways by showing that a network of intracellular TGF-β regulators, smads 7, 2, and 3, control β-cell proliferation after β-cell loss, and specifically, smad7 is necessary for that β-cell proliferation. Importantly, this smad7-mediated proliferation appears to entail passing through a transient, nonpathologic dedifferentiation of β-cells to a pancreatic polypeptide-fold hormone-positive state. TGF-β receptor II appears to be a receptor important for controlling the status of the smad network in β-cells. These studies should help our understanding of properly regulated β-cell replication.
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What OpenQuestion holds
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.