ArticleCells2021
DYRK1A Kinase Inhibitors Promote β-Cell Survival and Insulin Homeostasis.
Article in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 22 citations in OpenAlex.
- Design, Synthesis and Antihyperglycemic/Antilipidemic Activities of Quinoline-thiazolidine-2,4-dione Hybrid.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Design, synthesis and biological evaluation of quinazoline-carbazole derivatives as dual TXNIP/DYRK1A inhibitors for the treatment of type 2 diabetes mellitus.Molecular diversity · 2026Article
- Leucettinib-21 decreases dosage effects of DYRK1A in human trisomy 21 induced pluripotent stem cell-derived neural cells.Disease models & mechanisms · 2026Article
- Leucettinib-21 decreases dosage effects of DYRK1A in human trisomy 21 iPSC-derived neural cells.bioRxiv : the preprint server for biology · 2026Article
- Species-specific sensitivity to intracerebroventricular streptozotocin in rats and mice highlights pathways and proteins relevant to Alzheimer's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2025Article
- Review
- WS6 and 5-iodotubercidin small molecules and growth factors; TGF, HGF, and EGF synergistically enhance proliferation of β-like human induced pluripotent stem cells (iPSCs).Journal of diabetes and metabolic disorders · 2024Article
- Targeting β-Cell Plasticity: A Promising Approach for Diabetes Treatment.Current issues in molecular biology · 2024Review
- Ameliorating and refining islet organoids to illuminate treatment and pathogenesis of diabetes mellitus.Stem cell research & therapy · 2024Review
- Targeting the DYRK1A kinase prevents cancer progression and metastasis and promotes cancer cells response to G1/S targeting chemotherapy drugs.NPJ precision oncology · 2024Article
- Modelling human diabetesFrontiers in endocrinology · 2024Review
- Binding mechanism and biological effects of flavone DYRK1A inhibitors for the design of new antidiabetics.Scientific reports · 2023Article
- Silmitasertib (CX-4945), a Clinically Used CK2-Kinase Inhibitor with Additional Effects on GSK3β and DYRK1A Kinases: A Structural Perspective.Journal of medicinal chemistry · 2023Article
- Article
- The Omnipresence of DYRK1A in Human Diseases.International journal of molecular sciences · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
The rising prevalence of diabetes is threatening global health. It is known not only for the occurrence of severe complications but also for the SARS-Cov-2 pandemic, which shows that it exacerbates susceptibility to infections. Current therapies focus on artificially maintaining insulin homeostasis, and a durable cure has not yet been achieved. We demonstrate that our set of small molecule inhibitors of DYRK1A kinase potently promotes β-cell proliferation, enhances long-term insulin secretion, and balances glucagon level in the organoid model of the human islets. Comparable activity is seen in INS-1E and MIN6 cells, in isolated mice islets, and human iPSC-derived β-cells. Our compounds exert a significantly more pronounced effect compared to harmine, the best-documented molecule enhancing β-cell proliferation. Using a body-like environment of the organoid, we provide a proof-of-concept that small-molecule-induced human β-cell proliferation via DYRK1A inhibition is achievable, which lends a considerable promise for regenerative medicine in T1DM and T2DM treatment.
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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.