Abstract

Chronic inflammation is a hallmark of diabetes mellitus and a key driver of its long-term complications. 
Hyperglycaemia triggers a cascade of molecular and cellular events that disrupt immune homeostasis, promote 
persistent low-grade inflammation, and impair resolution pathways. This review synthesizes current 
understanding of the mechanisms linking elevated glucose levels to immune dysregulation, including advanced 
glycation end product (AGE) formation, oxidative stress, metabolic reprogramming of immune cells, 
inflammasome activation, and dysregulated cytokine networks. We discuss how these processes converge to 
sustain chronic inflammation, contribute to insulin resistance, endothelial dysfunction, and tissue damage in 
organs such as the vasculature, kidneys, liver, nerves, and retina. We also examine emerging biomarkers of 
inflammatory activity in diabetes and evaluate therapeutic strategies targeting inflammatory pathways, including 
glycaemic control, anti-inflammatory agents, immune modulators, and lifestyle interventions. A clearer 
understanding of how hyperglycaemia orchestrates immune dysfunction will enhance prevention and treatment of 
diabetic complications and inform precision medicine approaches.