ArticleCell death & disease2025
IL-1β priming triggers an adaptive stress response that enhances pancreatic β-cell resilience to subsequent cytotoxic inflammatory insult.
Article in Cell death & disease, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- From xanthine oxidase inhibition to inflammasome regulation: exploring the potential role of allopurinol in TXNIP-NLRP3 signaling and pyroptosis in diabetes.Inflammopharmacology · 2026Review
- Urinary Extracellular Vesicle-Derived miRNAs as Regulators and Biomarkers in Diabetic Kidney Disease.International journal of molecular sciences · 2026Review
- Metabolic-inflammatory memory: the common pathological basis and therapeutic targets of metabolic syndrome.Reviews in endocrine & metabolic disorders · 2026Review
- Dendritic Cells as Immunometabolic Regulatory Nodes in Diabetes: Molecular Mechanisms and Therapeutic Reprogramming.International journal of molecular sciences · 2026Review
- Review
- Mitochondria-associated programmed cell death in pancreatic β cell of T2DM.Apoptosis : an international journal on programmed cell death · 2026Review
- Evidence for a Cytokine-Sensitive Network of Iron-Associated Genes That Protects Pancreatic Islets Against Ferroptosis.Metabolites · 2026Article
- Gut microbiota in type 2 diabetes mellitus: mechanistic links between dysbiosis, insulin resistance, and chronic low-grade inflammation.Frontiers in endocrinology · 2026Review
- Neoepitopes at the crossroads of immunometabolism: metabolic remodeling of antigen presentation in type 1 diabetes.Frontiers in immunology · 2026Review
- Artificial intelligence-driven therapeutics for disease modification in type 1 diabetes: a digital public health and clinical translation framework.Frontiers in public health · 2026Review
- Stress-driven remodeling of antigen presentation and chemokine signaling in pancreatic β-cells: implications for type 1 diabetes.Frontiers in immunology · 2026Review
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Authors and funding
9 authors.
Funding
Abstract
Pancreatic β-cells fine-tune glucose homeostasis through insulin secretion. The endoplasmic reticulum (ER) is critical for insulin production, relying on the unfolded protein response (UPR) to adapt to the body's fluctuating demands. Islets from both type 1 (T1D) and type 2 diabetes (T2D) exhibit inflammation, β-cell dysfunction, and loss. ER stress is present in the inflamed islets of autoimmune diabetes-prone mice and individuals with T1D and T2D. Inflammatory cytokines induce ER stress and disrupt UPR regulation, driving β-cell apoptosis and contributing to diabetes development. Inflammatory cytokines, e.g., IL-1β, impair β-cell function and survival, contributing to diabetes pathogenesis by inducing stress, altering gene expression, driving dedifferentiation, and reducing insulin production. Paradoxically, β-cells exhibit a high density of IL-1R1, and IL-1R1/KO mice display impaired glucose tolerance and reduced insulin secretion. Postprandial IL-1β secreted by macrophages helps maintain blood glucose homeostasis. These observations suggest that circulating low IL-1β concentrations may have physiologically relevant roles; however, their effects on β-cell function and survival remain unclear due to conflicting reports. Preconditioning β-cells with physiological circulating levels of IL-1β (IL-1β
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