ArticleJournal of molecular medicine (Berlin, Germany)2011
Cytokine toxicity in insulin-producing cells is mediated by nitro-oxidative stress-induced hydroxyl radical formation in mitochondria.
Article in Journal of molecular medicine (Berlin, Germany), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 70 citations in OpenAlex.
- The Potential Roles of Oral Hypoglycemic Agents to Modulate Mitochondrial Function in Type 1 Diabetes Mellitus: A Scoping Review.Life (Basel, Switzerland) · 2026Review
- Preventing the onset of diabetes with precision delivery of mesenchymal stem cells to the pancreas in a preclinical model.Stem cell research & therapy · 2025Article
- Type 1 Diabetes Mellitus and Vitamin D.International journal of molecular sciences · 2025Review
- Glucose-Lowering Effects of Imeglimin and Its Possible Beneficial Effects on Diabetic Complications.Biology · 2023Review
- Ferroptosis Signaling in Pancreatic β-Cells: Novel Insights & Therapeutic Targeting.International journal of molecular sciences · 2022Review
- Review
- To Be or Not to Be: The Divergent Action and Metabolism of Sphingosine-1 Phosphate in Pancreatic Beta-Cells in Response to Cytokines and Fatty Acids.International journal of molecular sciences · 2022Review
- Islet Lymphocytes Maintain a Stable Regulatory Phenotype Under Homeostatic Conditions and Metabolic Stress.Frontiers in immunology · 2022Article
- Chemical inducer of regucalcin attenuates lipopolysaccharide-induced inflammatory responses in pancreatic MIN6 β-cells and RAW264.7 macrophages.FEBS open bio · 2022Article
- Oxidative stress-mediated beta cell death and dysfunction as a target for diabetes management.Frontiers in endocrinology · 2022Review
- Circadian rhythms and pancreas physiology: A review.Frontiers in endocrinology · 2022Review
- Mitochondrial Oxidative Stress-A Causative Factor and Therapeutic Target in Many Diseases.International journal of molecular sciences · 2021Review
- Dissecting in vivo and in vitro redox responses using chemogenetics.Free radical biology & medicine · 2021Review
- Insulin resistance in diabetes: The promise of using induced pluripotent stem cell technology.World journal of stem cells · 2021Review
- A Review of Current Trends with Type 2 Diabetes Epidemiology, Aetiology, Pathogenesis, Treatments and Future Perspectives.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Review
- Scientific Advances in Diabetes: The Impact of the Innovative Medicines Initiative.Frontiers in medicine · 2021Review
- The Role of Thioredoxin/Peroxiredoxin in the β-Cell Defense Against Oxidative Damage.Frontiers in endocrinology · 2021Review
- Oxidative Stress in Cytokine-Induced Dysfunction of the Pancreatic Beta Cell: Known Knowns and Known Unknowns.Metabolites · 2020Review
- Review
- MCPIP1 regulates the sensitivity of pancreatic beta-cells to cytokine toxicity.Cell death & disease · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although nitric oxide (NO) and oxidative stress both contribute to proinflammatory cytokine toxicity in pancreatic β-cells during type 1 diabetes mellitus (T1DM) development, the interactions between NO and reactive oxygen species (ROS) in cytokine-mediated β-cell death have not been clarified. Exposure of insulin-producing RINm5F cells to IL-1β generated NO, while exposure to a combination of IL-1β, TNF-α, and IFN-γ, which simulates T1DM conditions, generated both NO and ROS. In theory, two reactions between NO and ROS are possible, one with the superoxide radical yielding peroxynitrite, and the other with hydrogen peroxide (H(2)O(2)) yielding hydroxyl radicals. Results of the present work exclude peroxynitrite involvement in cytokine toxicity to β-cells because its generation did not correlate with the toxic action of cytokines. On the other hand, we show that H(2)O(2), produced upon exposure of insulin-producing cell clones and primary rat islet cells to cytokines almost exclusively in the mitochondria, reacted in the presence of trace metal (Fe(++)) with NO forming highly toxic hydroxyl radicals, thus explaining the severe toxicity that causes apoptotic β-cell death. Expression of the H(2)O(2)-inactivating enzyme catalase in mitochondria protected against cytokine toxicity by preventing hydroxyl radical formation. We therefore conclude that proinflammatory cytokine-mediated β-cell death is due to nitro-oxidative stress-mediated hydroxyl radical formation in the mitochondria.
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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.