ArticleCell death & disease2022
Mutated lncRNA increase the risk of type 2 diabetes by promoting β cell dysfunction and insulin resistance.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 13 citations in OpenAlex.
- Mettl14-mediated mJournal of endocrinological investigation · 2026Article
- From In Silico to Clinic: Harnessing Noncoding RNAs for Diabetes Research and Therapy, a Step toward ncRNA Precision.ACS pharmacology & translational science · 2026Review
- Look Who Is Talking: Extracellular Vesicles as Mediators of Intercellular and Interorgan Communication.Comprehensive Physiology · 2026Review
- Harnessing exosomal long non-coding RNAs as a new frontier for molecular diagnostics and therapeutics in diabetes mellitus.Cell communication and signaling : CCS · 2026Review
- Circulating long non-coding RNAs as predictors of type 2 diabetes mellitus development: results from the CORDIOPREV study.Cardiovascular diabetology · 2025Article
- The impact of ncRNAs on type 2 diabetes: A comprehensive review covering molecular mechanisms to clinical applications.Molecular therapy. Nucleic acids · 2025Review
- Stress-Related LncRNAs and Their Roles in Diabetes and Diabetic Complications.International journal of molecular sciences · 2025Review
- PTBP1 as a potential regulator of disease.Molecular and cellular biochemistry · 2024Review
- PARN Maintains RNA Stability to Regulate Insulin Maturation and GSIS in Pancreatic β Cells.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The Role of Extracellular Vesicles in Metabolic Diseases.Biomedicines · 2024Review
- LncRNA as a regulator in the development of diabetic complications.Frontiers in endocrinology · 2024Review
- Extracellular vesicle-mediated intercellular and interorgan crosstalk of pancreatic islet in health and diabetes.Frontiers in endocrinology · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Islet β cell dysfunction and insulin resistance are the main pathogenesis of type 2 diabetes (T2D), but the mechanism remains unclear. Here we identify a rs3819316 C > T mutation in lncRNA Reg1cp mainly expressed in islets associated with an increased risk of T2D. Analyses in 16,113 Chinese adults reveal that Mut-Reg1cp individuals had higher incidence of T2D and presented impaired insulin secretion as well as increased insulin resistance. Mice with islet β cell specific Mut-Reg1cp knock-in have more severe β cell dysfunction and insulin resistance. Mass spectrometry assay of proteins after RNA pulldown demonstrate that Mut-Reg1cp directly binds to polypyrimidine tract binding protein 1 (PTBP1), further immunofluorescence staining, western blot analysis, qPCR analysis and glucose stimulated insulin secretion test reveal that Mut-Reg1cp disrupts the stabilization of insulin mRNA by inhibiting the phosphorylation of PTBP1 in β cells. Furthermore, islet derived exosomes transfer Mut-Reg1cp into peripheral tissue, which then promote insulin resistance by inhibiting AdipoR1 translation and adiponectin signaling. Our findings identify a novel mutation in lncRNA involved in the pathogenesis of T2D, and reveal a new mechanism for the development of T2D.
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