Oxidative Stress and Inflammation in Type 2 Diabetes: Pathways to Organ Complications

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About this Research Topic

This Research Topic is closed for submissions.

Background

Chronic low-grade inflammation and oxidative stress are now recognized as central mechanisms in the development and progression of diabetic complications. In type 2 diabetes, persistent redox imbalance and pro-inflammatory pathways drive structural and functional damage in various organs, including the kidneys, heart, vasculature, and liver.

The goal of this Research Topic is to explore the clinical and mechanistic links between redox imbalance, inflammatory pathways, and organ dysfunction in patients with type 2 diabetes. By encouraging contributions from both clinical and basic research, we aim to highlight emerging biomarkers, mechanistic insights, and novel therapeutic approaches that target these interrelated pathways.

Suitable themes include:
• Oxidative stress biomarkers and clinical relevance in type 2 diabetes
• Inflammatory mediators and cytokine networks as predictors of organ damage
• Redox-inflammatory pathways in diabetic nephropathy, cardiomyopathy, or NAFLD
• Mitochondrial dysfunction, mitohormesis, and organ stress modulation
• Therapeutic interventions targeting oxidative stress and inflammation, including pharmacological, nutraceutical, and lifestyle approaches
• Translational studies linking redox biology to clinical outcomes
• Emerging strategies for risk stratification using integrated redox and inflammatory markers
• Comparative effects of different antidiabetic agents on redox balance and inflammation
• Mechanistic studies and small trials exploring novel targets or biomarkers

Disclosure: Topic Editor Keizo Kanasaki has collaborations with Boehringer Ingelheim, Taisho Pharmaceutical, Bayer, Mitsubishi Tanabe Pharma, and Kowa.

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Keywords: Type 2 diabetes, oxidative stress, inflammation, diabetic complications, organ dysfunction, redox balance, mitohormesis, cardiovascular disease, renal disease, biomarkers

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