ReviewFrontiers in genetics2017
Evidence for Loss in Identity, De-Differentiation, and
Review in Frontiers in genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Global prevalence of erectile dysfunction and its associated risk factors among men with type 1 diabetes: a systematic review and meta-analysis.International journal of impotence research · 2024Pooled it
- Presenilin-1 controls glycolysis and identity of pancreatic beta cells.Communications biology · 2026Article
- eNAMPT induces alpha-cell mass expansion but impaired glucagon counter regulatory response.Endocrinology · 2026Article
- Stimulation to secrete insulin induces pancreatic β-cell dysfunction through Tfe3 activation.iScience · 2026Article
- IL-1β priming triggers an adaptive stress response that enhances pancreatic β-cell resilience to subsequent cytotoxic inflammatory insult.Cell death & disease · 2025Article
- Human pancreatic α-cell heterogeneity and trajectory inference analyses reveal SMOC1 as a β-cell dedifferentiation gene.Nature communications · 2025Article
- The Islet-1 Interaction Partner Rnf20 Regulates Glucose Homeostasis and Pancreatic β-Cell Identity.Diabetes · 2025Article
- Loss of β-cell identity in human islets treated with glibenclamide.Diabetes, obesity & metabolism · 2025Article
- Single-cell analysis of oxidative phosphorylation protein expression in pancreatic islets in type 2 diabetes.The Journal of endocrinology · 2025Article
- Osteocalcin induces phosphorylation of FOXO1 in human beta-cells and restores insulin expression under hyperglycemic conditions.Research square · 2025Article
- Post translational modification regulation of transcription factors governing pancreatic β-cell identity and functional mass.Frontiers in endocrinology · 2025Review
- Obesity's systemic impact: exploring molecular and physiological links to diabetes, cardiovascular disease, and heart failure.Frontiers in endocrinology · 2025Review
- Mesangiogenic progenitor cells: a mesengenic and vasculogenic branch of hemopoiesis? A story of neglected plasticity.Frontiers in cell and developmental biology · 2025Article
- Harnessing beta-cell replication: advancing molecular insights to regenerative therapies in diabetes.Frontiers in endocrinology · 2025Review
- Repression of latent NF-κB enhancers by PDX1 regulates β cell functional heterogeneity.Cell metabolism · 2024Article
- Advanced therapy to cure diabetes: mission impossible is now possible?Frontiers in cell and developmental biology · 2024Review
- Ghrelin deletion and conditional ghrelin cell ablation increase pancreatic islet size in mice.The Journal of clinical investigation · 2023Article
- Species-specific roles for the MAFA and MAFB transcription factors in regulating islet β cell identity.JCI insight · 2023Article
- 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
- CLEC11A improves insulin secretion and promotes cell proliferation in human beta-cells.Journal of molecular endocrinology · 2023Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
The two main types of diabetes mellitus have distinct etiologies, yet a similar outcome: loss of islet β-cell function that is solely responsible for the secretion of the insulin hormone to reduce elevated plasma glucose toward euglycemic levels. Type 1 diabetes (T1D) has traditionally been characterized by autoimmune-mediated β-cell death leading to insulin-dependence, whereas type 2 diabetes (T2D) has hallmarks of peripheral insulin resistance, β-cell dysfunction, and cell death. However, a growing body of evidence suggests that, especially during T2D, key components of β-cell failure involves: (1) loss of cell identity, specifically proteins associated with mature cell function (e.g., insulin and transcription factors like MAFA, PDX1, and NKX6.1), as well as (2) de-differentiation, defined by regression to a progenitor or stem cell-like state. New technologies have allowed the field to compare islet cell characteristics from normal human donors to those under pathophysiological conditions by single cell RNA-Sequencing and through epigenetic analysis. This has revealed a remarkable level of heterogeneity among histologically defined "insulin-positive" β-cells. These results not only suggest that these β-cell subsets have different responses to insulin secretagogues, but that defining their unique gene expression and epigenetic modification profiles will offer opportunities to develop cellular therapeutics to enrich/maintain certain subsets for correcting pathological glucose levels. In this review, we will summarize the recent literature describing how β-cell heterogeneity and plasticity may be influenced in T2D, and various possible avenues of therapeutic intervention.
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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.