ArticleEndocrine2022
miR-25 and miR-92b regulate insulin biosynthesis and pancreatic β-cell apoptosis.
Article in Endocrine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 14 citations in OpenAlex.
- Mitochondrial Homeostasis in Pancreatic β Cell Function: Mechanisms and Therapeutic Targets for Diabetes.Journal of diabetes · 2026Review
- The impact of ncRNAs on type 2 diabetes: A comprehensive review covering molecular mechanisms to clinical applications.Molecular therapy. Nucleic acids · 2025Review
- In Silico Analysis of Possible microRNAs Involved in the Pathogenesis of White-Nose Syndrome inInternational journal of molecular sciences · 2025Article
- Microbial and proteomic signatures of type 2 diabetes in an Arab population.Journal of translational medicine · 2024Article
- Downregulation ofJournal of clinical medicine research · 2024Article
- Targeting β-Cell Plasticity: A Promising Approach for Diabetes Treatment.Current issues in molecular biology · 2024Review
- MicroRNAs in chronic pediatric diseases (Review).Experimental and therapeutic medicine · 2024Review
- Non-invasive diagnostic potential of salivary miR-25-3p for periodontal disease and osteoporosis among a cohort of elderly patients with type 2 diabetes mellitus.BMC oral health · 2023Article
- iPSC-Derived Pancreatic Progenitors Lacking FOXA2 Reveal Alterations in miRNA Expression Targeting Key Pancreatic Genes.Stem cell reviews and reports · 2023Article
- Non-coding RNAs in diabetes mellitus and diabetic cardiovascular disease.Frontiers in endocrinology · 2022Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposePancreatic β-cell failure is a central hallmark of the pathogenesis of diabetes mellitus; however, the molecular basis underlying chronic inflammation-caused β-cell failure remains unclear. This study reported here specifically assessed the association between miR-25/miR-92b family and β-cell failure in diabetes.
methodsIL-1β and two additional ER stress activators, palmitate and tunicamycin were applied to evaluate the expression level miR-25 by Taqman
resultsmiRNA ChIP identified the increased level of miR-25 in INS-1 cells by IL-1β treatment. Expression levels of miR-25 were significantly upregulated with the treatment of IL-1β, palmitate or tunicamycin in both INS-1 cells and human islets. Ectopic elevation of miR-25 recapitulated most featured β-cell defects caused by IL-1β, including inhibition of insulin biosynthesis and increased β-cell apoptosis. These detrimental effects of miR-25 relied on its seed sequence recognition and repressed expression of its target genes Neurod1 and Mcl1. The miR-25/NEUROD1 axis reduced insulin biosynthesis via transcriptional regulation of β-cell specific genes. The miR-25/MCL1 axis caused β-cell apoptosis in a CASPASE-3/PARP1-dependent manner. Comparable impairments were generated by miR-92b and miR-25, emphasizing the redundant biological roles of miRNA family members with the same seed sequence.
conclusionMiR-25/miR-92b family plays a major role in β-cell failure occurring under inflammation and diabetes states.
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