Neutrophil-Linked Inflammatory Mechanisms and Biomarkers in Diabetic Microvascular Complications

Diabetic microvascular complications, including nephropathy, retinopathy, and neuropathy, are major causes of morbidity in diabetes. Increasing evidence highlights neutrophils as key contributors to the chronic inflammatory processes underlying these complications. In the diabetic environment, neutrophils exhibit impaired recruitment, defective phagocytosis, dysregulated degranulation, and excessive production of reactive oxygen species and neutrophil extracellular traps (NETs). These dysfunctions not only reduce pathogen clearance but also exacerbate tissue injury through persistent low-grade inflammation. Furthermore, neutrophils interact with other immune cells, such as macrophages, dendritic cells, T cells, and B cells, perpetuating immune imbalance and tissue damage. Various neutrophil-derived cytokines and granular proteins also influence vascular permeability and endothelial dysfunction. In recent years, neutrophil-related biomarkers-such as absolute neutrophil count, neutrophil-to-lymphocyte ratio, platelet-to-neutrophil ratio, and systemic immune-inflammation index-have gained attention as accessible and cost-effective tools for predicting and monitoring diabetic microvascular complications. This review summarizes the multifaceted roles of neutrophils in the pathogenesis of diabetic microvascular disease and highlights emerging clinical applications of neutrophil-based inflammatory biomarkers. A better understanding of neutrophil-driven mechanisms may open new avenues for early diagnosis, therapeutic intervention, and personalized care in diabetic patients.