ArticleiScience2024
Complement C3 promotes islet β-cell dedifferentiation by activating Wnt/β-catenin pathway.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 6 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
6 citing papers in PubMed.
- Beta-cell-specific C3 deficiency exacerbates metabolic dysregulation and insulin resistance in obesity.Molecular metabolism · 2026Article
- Early elevation of complement-related proteins in metabolic dysfunction-associated steatotic liver disease (MASLD) with normal liver enzymes.BMC gastroenterology · 2025Article
- Islet-intrinsic sex differences in inflammatory signaling contribute to autoimmune diabetes susceptibility.bioRxiv : the preprint server for biology · 2025Article
- INS2 lineage cell tracking and insulin expression in the related organs of mice.Scientific reports · 2025Article
- Single and Combined Impact of Semaglutide, Tirzepatide, and Metformin on β-Cell Maintenance and Function Under High-Glucose-High-Lipid Conditions: A Comparative Study.International journal of molecular sciences · 2025Article
- Obesity's systemic impact: exploring molecular and physiological links to diabetes, cardiovascular disease, and heart failure.Frontiers in endocrinology · 2025Review
Corrections and comments
- Retracted
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Islet β-cell dedifferentiation is a key step in the progression of diabetes, and complement C3 enhances secretion of several inflammatory mediators and cytokines in type 2 diabetes mellitus (T2DM). Here, we identified the underlying mechanisms of complement C3 in islet β-cell dedifferentiation. The protein level of C3 is increased in blood of T2DM patients and mice, as well as in T2DM islet β cells. Insulin, gliclazide, and metformin decreased complement C3, Nga3, and Oct4 levels but increased Pdx1 and MafA expressions; these treatments inhibit islet β-cell dedifferentiation in
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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.