ReviewFrontiers in immunology2025
The role of oxidative post-translational modifications in type 1 diabetes pathogenesis.
Review in Frontiers in immunology, 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.
- Beta Cell Stress to Epitope Diversification: Post-Translationally Modified Antigens in Type 1 Diabetes.Immunological reviews · 2026Review
- Oxidative Stress Biomarkers in Pediatric and Early-Stage Type 1 Diabetes: Toward Redox Phenotyping.Antioxidants (Basel, Switzerland) · 2026Review
- Oxidative Post-Translational Modifications of Insulin in Type 1 Diabetes Autoimmunity.Immunological reviews · 2026Review
- From Disposal to Display: Crinophagy as a β-Cell Source of Neoantigens in Type 1 Diabetes.Immunological reviews · 2026Review
- Structural Remodeling of TCR-HLA-DQ8 Recognition by a β-Cell Stress-Associated C19S Insulin Neoepitope in Type 1 Diabetes.International journal of molecular sciences · 2026Article
- Succinylation modification in diabetes and diabetic complications: Mechanisms and functions (Review).Molecular medicine reports · 2026Review
- The rise and fall of a paradigm and conceiving a new hypothesis for type 1 diabetes. Reply to Nerup J, Lernmark A [letter].Diabetologia · 2026Article
- Rapid protein carbonylation and decreased insulin secretion induced by inflammatory oxidative stress compounds.Free radical biology & medicine · 2026Article
- Neoepitopes at the crossroads of immunometabolism: metabolic remodeling of antigen presentation in type 1 diabetes.Frontiers in immunology · 2026Review
- Scars of oxidative stress: protein carbonylation and beta cell dysfunction in diabetes.Frontiers in endocrinology · 2025Review
- Lymphedema pathogenesis involves antigen-driven expansion of CD4+ T cells in skin.Frontiers in immunology · 2025Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of type 1 diabetes (T1D) involves a complex interplay of genetic predisposition, immune processes, and environmental factors, leading to the selective destruction of pancreatic beta-cells by the immune system. Emerging evidence suggests that intrinsic beta-cell factors, including oxidative stress and post-translational modifications (PTM) of beta-cell antigens, may also contribute to their immunogenicity, shedding new light on the multifaceted pathogenesis of T1D. Over the past 30 years, neoepitopes generated by PTMs have been hypothesized to play a role in T1D pathogenesis, but their involvement has only been systematically investigated in recent years. In this review, we explored the interplay between oxidative PTMs, neoepitopes, and T1D, highlighting oxidative stress as a pivotal factor in immune system dysfunction, beta-cell vulnerability, and disease onset.
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Registered trials
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