ArticleGene therapy2014
Stable insulin-secreting ducts formed by reprogramming of cells in the liver using a three-gene cocktail and a PPAR agonist.
Article in Gene therapy, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
18 citing papers in PubMed, 45 citations in OpenAlex.
- The key regulation of LncRNA MALAT during reprogramming of primary mouse hepatocytes into insulin producing cells.Scientific reports · 2025Article
- Stem Cells Reprogramming in Diabetes Mellitus and Diabetic Complications: Recent Advances.Current diabetes reviews · 2025Review
- β-cell heterogeneity and molecular plasticity in type 2 diabetes: multi-omics perspectives and the role of gut microbiota.Frontiers in cell and developmental biology · 2025Review
- Forward programming of hiPSCs towards beta-like cells using Ngn3, Pdx1, and MafA.Scientific reports · 2024Article
- Development, regeneration, and physiological expansion of functional β-cells: Cellular sources and regulators.Frontiers in cell and developmental biology · 2024Review
- Harnessing gut cells for functional insulin production: Strategies and challenges.Biotechnology notes (Amsterdam, Netherlands) · 2023Review
- Alpha-to-beta cell trans-differentiation for treatment of diabetes.Biochemical Society transactions · 2021Review
- Improvement of the therapeutic capacity of insulin-producing cells trans-differentiated from human liver cells using engineered cell sheet.Stem cell research & therapy · 2021Article
- Transcription Factor Reprogramming in the Inner Ear: Turning on Cell Fate Switches to Regenerate Sensory Hair Cells.Frontiers in cellular neuroscience · 2021Article
- Mesenchymal Stem Cells: An Excellent Candidate for the Treatment of Diabetes Mellitus.International journal of endocrinology · 2021Review
- Article
- Liver to Pancreas Transdifferentiation.Current diabetes reports · 2019Review
- Reprogramming Cells to Make Insulin.Journal of the Endocrine Society · 2019Review
- Long-Term Correction of Diabetes in Mice by In Vivo Reprogramming of Pancreatic Ducts.Molecular therapy : the journal of the American Society of Gene Therapy · 2018Article
- PDX1, Neurogenin-3, and MAFA: critical transcription regulators for beta cell development and regeneration.Stem cell research & therapy · 2017Review
- Regenerative medicine and cell-based approaches to restore pancreatic function.Nature reviews. Gastroenterology & hepatology · 2017Review
- Reprogramming of Pancreatic Exocrine Cells AR42J Into Insulin-producing Cells Using mRNAs for Pdx1, Ngn3, and MafA Transcription Factors.Molecular therapy. Nucleic acids · 2016Article
- Identification of miRNAs Involved in Reprogramming Acinar Cells into Insulin Producing Cells.PloS one · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
With the long-term aim of developing a new type of therapy for diabetes, we have investigated the reprogramming of liver cells in normal mice toward a pancreatic phenotype using the gene combination Pdx1, Ngn3, MafA. CD1 mice were rendered diabetic with streptozotocin and given a single dose of Ad-PNM, an adenoviral vector containing all three genes. Ad-PNM induced hepatocytes of the liver to produce insulin, and the blood glucose became normalized. But over several weeks, the insulin-positive cells were lost and the blood glucose rose back to diabetic levels. Simultaneous administration of a peroxisome-proliferator-activated receptor agonist, WY14643, caused remission of diabetes at a lower dose of Ad-PNM and also caused the appearance of a population of insulin-secreting ductal structures in the liver. The insulin-positive ducts were stable and were able to relieve diabetes in the long term. We show that the effect of WY14643 is associated with the promotion of cell division of the ductal cells, which may increase their susceptibility to being reprogrammed toward a beta cell fate.
Indexed as
Identifiers
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.