ArticleMolecular metabolism2020
Single-cell transcriptomics of human islet ontogeny defines the molecular basis of β-cell dedifferentiation in T2D.
Article in Molecular metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 98 citations in OpenAlex.
- Human Islet miR-199a-5p and miR-214-3p Associate With Donor Age, BMI, and Sex and Mediate Cellular Aging in Islet-Derived Cells.Acta physiologica (Oxford, England) · 2026Article
- Workload-induced changes to cell state contribute to β-cell failure in diabetes.bioRxiv : the preprint server for biology · 2026Article
- Review
- Epigenetic adaptation of beta cells across lifespan and disease.Nature metabolism · 2026Article
- Single-Cell Multi-Omics in Type 2 Diabetes Mellitus: Revealing Cellular Heterogeneity and Mechanistic Insights.International journal of molecular sciences · 2025Review
- The role of the beta cell in type 2 diabetes: new findings from the last 5 years.Diabetologia · 2025Review
- Cell-type-specific cis-eQTLs in pancreatic cell types identify novel risk genes for type 2 diabetes.Briefings in bioinformatics · 2025Article
- Imeglimin suppresses glucagon secretion and induces a loss of α cell identity.Cell reports. Medicine · 2025Article
- Article
- 12-Lipoxygenase Inhibition Improves Glycemia and Obesity-associated Inflammation in Male Human Gene Replacement Mice.Endocrinology · 2025Article
- Identification of a vimentin-expressing α-cell phenotype in CF and normal pancreas.The Journal of endocrinology · 2025Article
- NKX2.2 and KLF4 cooperate to regulate α-cell identity.Genes & development · 2025Article
- Lessons from a model: early glucagon dysfunction in type 2 diabetes.Pflugers Archiv : European journal of physiology · 2025Article
- G6PC2 controls glucagon secretion by defining the set point for glucose in pancreatic α cells.Science translational medicine · 2025Article
- Single-Cell RNA-seq Analysis Reveals a Positive Correlation between Ferroptosis and Beta-Cell Dedifferentiation in Type 2 Diabetes.Biomedicines · 2024Article
- Regulation of endocrine cell alternative splicing revealed by single-cell RNA sequencing in type 2 diabetes pathogenesis.Communications biology · 2024Article
- HumanIslets: An integrated platform for human islet data access and analysis.bioRxiv : the preprint server for biology · 2024Article
- Advancing Diabetes Research: A Novel Islet Isolation Method from Living Donors.International journal of molecular sciences · 2024Article
- Pancreatic β-Cell Identity Change through the Lens of Single-Cell Omics Research.International journal of molecular sciences · 2024Review
- Islet-resident macrophage-derived miR-155 promotes β cell decompensation via targeting PDX1.iScience · 2024Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
objectiveDedifferentiation of pancreatic β-cells may reduce islet function in type 2 diabetes (T2D). However, the prevalence, plasticity and functional consequences of this cellular state remain unknown.
methodsWe employed single-cell RNAseq to detail the maturation program of α- and β-cells during human ontogeny. We also compared islets from non-diabetic and T2D individuals.
resultsBoth α- and β-cells mature in part by repressing non-endocrine genes; however, α-cells retain hallmarks of an immature state, while β-cells attain a full β-cell specific gene expression program. In islets from T2D donors, both α- and β-cells have a less mature expression profile, de-repressing the juvenile genetic program and exocrine genes and increasing expression of exocytosis, inflammation and stress response signalling pathways. These changes are consistent with the increased proportion of β-cells displaying suboptimal function observed in T2D islets.
conclusionsThese findings provide new insights into the molecular program underlying islet cell maturation during human ontogeny and the loss of transcriptomic maturity that occurs in islets of type 2 diabetics.
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