ArticleJournal of molecular cell biology2019
MicroRNA-24 promotes pancreatic beta cells toward dedifferentiation to avoid endoplasmic reticulum stress-induced apoptosis.
Article in Journal of molecular cell biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
- β-Cell Dedifferentiation in HOMA-βlow and HOMA-βhigh Subjects.The Journal of clinical endocrinology and metabolism · 2025Article
- microRNAs in Type 1 Diabetes: Roles, Pathological Mechanisms, and Therapeutic Potential.International journal of molecular sciences · 2025Review
- MicroRNA-24 therapeutic potentials in infarction, stroke, and diabetic complications.Molecular biology reports · 2024Review
- Article
- Advancing diabetes management: Exploring pancreatic beta-cell restoration's potential and challenges.World journal of gastroenterology · 2024Review
- Targeting β-Cell Plasticity: A Promising Approach for Diabetes Treatment.Current issues in molecular biology · 2024Review
- Insufficient TRPM5 Mediates Lipotoxicity-induced Pancreatic β-cell Dysfunction.Current medical science · 2024Article
- Decoding contextual crosstalk: revealing distinct interactions between non-coding RNAs and unfolded protein response in breast cancer.Cancer cell international · 2024Review
- Reduced miR-184-3p expression protects pancreatic β-cells from lipotoxic and proinflammatory apoptosis in type 2 diabetes via CRTC1 upregulation.Cell death discovery · 2022Article
- Article
- Role of the Transcription Factor MAFA in the Maintenance of Pancreatic β-Cells.International journal of molecular sciences · 2022Review
- MafA Regulation in β-Cells: From Transcriptional to Post-Translational Mechanisms.Biomolecules · 2022Review
- Knowledge domain and emerging trends in beta-cell research: A bibliometric and knowledge-map analysis.Frontiers in endocrinology · 2022Review
- The miR-200-Zeb1 axis regulates key aspects of β-cell function and survival in vivo.Molecular metabolism · 2021Article
- ERp29 forms a feedback regulation loop with microRNA-135a-5p and promotes progression of colorectal cancer.Cell death & disease · 2021Article
- M1 macrophage-derived exosomes impair beta cell insulin secretion via miR-212-5p by targeting SIRT2 and inhibiting Akt/GSK-3β/β-catenin pathway in mice.Diabetologia · 2021Article
- Circulating microRNAs Signature for Predicting Response to GLP1-RA Therapy in Type 2 Diabetic Patients: A Pilot Study.International journal of molecular sciences · 2021Article
- Targeting β-cell dedifferentiation and transdifferentiation: opportunities and challenges.Endocrine connections · 2021Review
- Non-Coding RNAs: Novel Players in Insulin Resistance and Related Diseases.International journal of molecular sciences · 2021Review
- Molecular Mechanisms of Apoptosis Induction and Its Regulation by Fatty Acids in Pancreatic β-Cells.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Current research indicates that beta cell loss in type 2 diabetes may be attributed to beta cell dedifferentiation rather than apoptosis; however, the mechanisms by which this occurs remain poorly understood. Our previous study demonstrated that elevation of microRNA-24 (miR-24) in a diabetic setting caused beta cell dysfunction and replicative deficiency. In this study, we focused on the role of miR-24 in beta cell apoptosis and dedifferentiation under endoplasmic reticulum (ER) stress conditions. We found that miR-24 overabundance protected beta cells from thapsigargin-induced apoptosis at the cost of accelerating the impairment of glucose-stimulated insulin secretion (GSIS) and enhancing the presence of dedifferentiation markers. Ingenuity® Pathway Analysis (IPA) revealed that elevation of miR-24 had an inhibitory effect on XBP1 and ATF4, which are downstream effectors of two key branches of ER stress, by inhibiting its direct target, Ire1α. Notably, elevated miR-24 initiated another pathway that targeted Mafa and decreased GSIS function in surviving beta cells, thus guiding their dedifferentiation under ER stress conditions. Our results demonstrated that the elevated miR-24, to the utmost extent, preserves beta cell mass by inhibiting apoptosis and inducing dedifferentiation. This study not only provides a novel mechanism by which miR-24 dominates beta cell turnover under persistent metabolic stress but also offers a therapeutic consideration for treating diabetes by inducing dedifferentiated beta cells to re-differentiation.
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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.