ArticleThe Journal of biological chemistry2019
MicroRNA-223 is essential for maintaining functional β-cell mass during diabetes through inhibiting both FOXO1 and SOX6 pathways.
Article in The Journal of biological chemistry, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.
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
37 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.
- Circulating microRNA as Biomarkers for Gestational Diabetes Mellitus-A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2023Pooled it
- Article
- Plasma Small Extracellular Vesicles of Ischemic Cardiomyopathy Aggravate Ventricular Remodeling Post-Myocardial Infarction and Promote miR-223-3p-mediated Dysfunction in Regulatory T Cells.Journal of cardiovascular translational research · 2025Article
- The impact of ncRNAs on type 2 diabetes: A comprehensive review covering molecular mechanisms to clinical applications.Molecular therapy. Nucleic acids · 2025Review
- Micro-223 Promotes Diabetic Osteoarthritis Progression by Regulating Cartilage Degeneration and Subchondral Bone Remodeling.Cartilage · 2025Article
- miR-223 alleviates DSS-induced colitis by prompting macrophage M2 polarization through PPAR-γ/FOXO1 signaling.Frontiers in immunology · 2025Article
- MiR-223-3p in Cancer Development and Cancer Drug Resistance: Same Coin, Different Faces.International journal of molecular sciences · 2024Review
- Targeting β-Cell Plasticity: A Promising Approach for Diabetes Treatment.Current issues in molecular biology · 2024Review
- A Novel "Endocrine Hormone": The Diverse Role of Extracellular Vesicles in Multiorgan Insulin Resistance.International journal of medical sciences · 2024Review
- Exercise increases MEF2A abundance in rat cardiac muscle by downregulating microRNA-223-5p.Scientific reports · 2023Article
- miRNAs in the Beta Cell-Friends or Foes?Endocrinology · 2023Review
- The link between glycemic control measures and eye microvascular complications in a clinical cohort of type 2 diabetes with microRNA-223-3p signature.Journal of translational medicine · 2023Article
- FoxO1 as a tissue-specific therapeutic target for type 2 diabetes.Frontiers in endocrinology · 2023Review
- The Role of Forkhead Box O in Pathogenesis and Therapy of Diabetes Mellitus.International journal of molecular sciences · 2022Review
- Maturation of beta cells: lessons from in vivo and in vitro models.Diabetologia · 2022Review
- Sox6, A Potential Target for MicroRNAs in Cardiometabolic Disease.Current hypertension reports · 2022Review
- Evaluation of muscle-specific and metabolism regulating microRNAs in a chronic swimming rat model.Journal of muscle research and cell motility · 2022Article
- The Temporal Profile of Circulating miRNAs during Gestation in Overweight and Obese Women with or without Gestational Diabetes Mellitus.Biomedicines · 2022Article
- Molecular study of the proliferation process of beta cells derived from pluripotent stem cells.Molecular biology reports · 2022Review
- Multi-Organ Crosstalk with Endocrine Pancreas: A Focus on How Gut Microbiota Shapes Pancreatic Beta-Cells.Biomolecules · 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
9 authors at 5 institutions in 3 countries.
Funding
Abstract
The initiation and development of diabetes are mainly ascribed to the loss of functional β-cells. Therapies designed to regenerate β-cells provide great potential for controlling glucose levels and thereby preventing the devastating complications associated with diabetes. This requires detailed knowledge of the molecular events and underlying mechanisms in this disorder. Here, we report that expression of microRNA-223 (miR-223) is up-regulated in islets from diabetic mice and humans, as well as in murine Min6 β-cells exposed to tumor necrosis factor α (TNFα) or high glucose. Interestingly, miR-223 knockout (KO) mice exhibit impaired glucose tolerance and insulin resistance. Further analysis reveals that miR-223 deficiency dramatically suppresses β-cell proliferation and insulin secretion. Mechanistically, using luciferase reporter gene assays, histological analysis, and immunoblotting, we demonstrate that miR-223 inhibits both forkhead box O1 (FOXO1) and SRY-box 6 (SOX6) signaling, a unique bipartite mechanism that modulates expression of several β-cell markers (pancreatic and duodenal homeobox 1 (PDX1), NK6 homeobox 1 (NKX6.1), and urocortin 3 (UCN3)) and cell cycle-related genes (cyclin D1, cyclin E1, and cyclin-dependent kinase inhibitor P27 (P27)). Importantly, miR-223 overexpression in β-cells could promote β-cell proliferation and improve β-cell function. Taken together, our results suggest that miR-223 is a critical factor for maintaining functional β-cell mass and adaptation during metabolic stress.
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.