ArticleNature communications2025
Human pancreatic α-cell heterogeneity and trajectory inference analyses reveal SMOC1 as a β-cell dedifferentiation gene.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Harnessing Endogenous Plasticity Rather than Reprogramming of Mature Cells Will Advance Regenerative Medicine, Cancer Treatment and Rejuvenation.Stem cell reviews and reports · 2026Review
- The central role of the β-cell in diabetes: from monogenic forms to type 1, type 2, and gestational diabetes.Reviews in endocrine & metabolic disorders · 2026Review
- Review
- Variation in the Circulating Levels of Retinoic Acid and Type 2 Diabetes: Relationships with Glycemic Control Indices, Disease Treatment and Complications.Diagnostics (Basel, Switzerland) · 2026Article
- Reuniting diabetes through the islet coordinate framework.The lancet. Diabetes & endocrinology · 2026Article
- Stress-driven remodeling of antigen presentation and chemokine signaling in pancreatic β-cells: implications for type 1 diabetes.Frontiers in immunology · 2026Review
- Scars of oxidative stress: protein carbonylation and beta cell dysfunction in diabetes.Frontiers in endocrinology · 2025Review
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Authors and funding
11 authors.
Funding
Abstract
β-cell dysfunction and dedifferentiation towards an α-cell-like phenotype are hallmarks of type 2 diabetes. However, the cell subtypes involved in β-to-α-cell transition are unknown. Using single-cell and single-nucleus RNA-seq, RNA velocity, PAGA/cell trajectory inference, and gene commonality, we interrogated α-β-cell fate switching in human islets. We found five α-cell subclusters with distinct transcriptomes. PAGA analysis showed bifurcating cell trajectories in non-diabetic while unidirectional cell trajectories from β-to-α-cells in type 2 diabetes islets suggesting dedifferentiation towards α-cells. Ten genes comprised the common signature genes in trajectories towards α-cells. Among these, the α-cell gene SMOC1 was expressed in β-cells in type 2 diabetes. Enhanced SMOC1 expression in β-cells decreased insulin expression and secretion and increased β-cell dedifferentiation markers. Collectively, these studies reveal differences in α-β-cell trajectories in non-diabetes and type 2 diabetes human islets, identify signature genes for β-to-α-cell trajectories, and discover SMOC1 as an inducer of β-cell dysfunction and dedifferentiation.
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