Abstract: Diabetic retinopathy (DR) is a retinal microvascular complication that arises with the prolongation of the disease in diabetic patients. Its main pathological changes include retinal inflammation, increased vascular permeability, and abnormal retinal surface angiogenesis. Multiple mechanisms are involved in the development of DR, and oxidative stress is an important mechanism in its development, which includes the polyol pathway, advanced glycation end products (AGEs) pathway, the hexosamine pathway (HBP), the protein kinase C (PKC) pathway, and the angiotensin II (ANG II) pathway. The initiation of oxidative stress triggers an intracellular cascade reaction that generates excessive reactive oxygen species. Excessive reactive oxygen species lead to protein modification, inflammatory response, apoptosis, dysregulation of autophagy, impaired mitochondrial function, interfering with a variety of signaling pathways and affecting a variety of biological processes, which result in the onset and progression of DR. Further study of these interactions is important for understanding the pathogenesis of DR and finding relevant therapeutic strategies.

Key words: diabetic retinopathy, inflammation, oxidative stress