Diabetes mellitus is a complex metabolic disease caused by high blood glucose and urine sugar due to insulin insufficiency or insulin dysregulation, and is a systemic, chronic and progressive disease. For a long time, due to the discovery and application of insulin, the successive introduction of various hypoglycemic drugs, and the widespread use of various antibiotics, the number of deaths due to acute complications and co-infections in diabetes has been greatly reduced, and the life expectancy of patients has been prolonged, but the incidence of chronic complications of diabetes has increased accordingly. Diabetic retinopathy is one of the most common complications of diabetes mellitus and is a major cause of blindness. This article briefly describes the pathogenesis of diabetic retinopathy as follows. In recent years, although some progress has been made in the study of the pathogenesis of diabetic retinopathy, no clear conclusion has been reached. It is generally believed that the occurrence of diabetic retinopathy is the result of the synergistic effect of several factors. First of all, hyperglycemia is closely related to diabetic retinopathy, and it is likely to be one of the main mechanisms for the occurrence and development of retinopathy in diabetic patients. There is no definite conclusion on the relationship between hyperglycemia and the occurrence of diabetic retinopathy, but a large amount of information confirms that the higher the blood glucose level of diabetic patients, the greater the frequency of diabetic microangiopathy. Epidemiological surveys have shown that approximately 75% to 80% of diabetic patients who do not pay attention to glycemic control develop diabetic retinopathy within 15 years of onset. Most mathematicians believe that the development of diabetic retinopathy is the result of long-term hyperglycemia. The late complications of diabetes are due to chronic hyperglycemia acting on different metabolic pathways. In different organ tissues, the affected metabolic pathways can be partially or completely different. In some patients with very good glycemic control, complications progress rapidly, while others with poor glycemic control progress slowly or even without complications, related to the different activity of metabolic pathways in these patients. Different tissues and organs have different metabolic pathways and different enzyme activities, resulting in different susceptibility of certain organs to the occurrence of diabetic complications. Second, the amount of late glycosylation end-products aggregation is closely related to the severity of diabetic retinopathy. According to in-depth studies in recent years, the accumulation of excessive late glycosylation end-products in the body caused by long-term hyperglycemia may lead to chronic lesions and loss of function in various systems. When the glucose concentration in blood is elevated, reversible early glycation products can be formed with proteins, and the higher the glucose concentration, the more early glycation products are formed. With normal blood glucose control, the early glycation products can be reduced to normal. However, some early glycation products located on collagen and other proteins in the vessel wall do not degrade, but form irreversible late glycosylation end products through a slow and complex chemical rearrangement. Although blood glucose has been controlled normally, the late glycosylation end products cannot be restored to normal levels and form a large number of binding proteins, which may cause changes in the structure and function of the vessel wall, proliferation of vascular endothelial cells and narrowing of the vessels. Third, blood rheology dysregulation leading to slowed blood flow in the microvasculature and its damage to the vessel wall play an important role in diabetic retinopathy. In diabetic patients, the mobility and deformability of red blood cells are decreased and the aggregation of red blood cells is significantly higher than normal, which interferes with the flow of red blood cells in capillaries and small veins, causing physical damage to the vessel wall, and can also block capillaries, causing damage due to hypoxia. The deformability of leukocytes in diabetic patients is significantly lower than normal, platelet adhesion is enhanced, aggregation is increased, and there is a slight increase in serum viscosity. These abnormal platelet adhesion and cohesion as well as leukocyte adhesion and infiltration may be important causes of capillary occlusion, resulting in retinal tissue ischemia and hypoxia, which becomes the main cause of diabetic retinopathy. Fourth, endocrine substances released by retinal microvascular endothelial cell injury may play an important role in the development of diabetic retinopathy. The retinal microvasculature consists of three major components: pericytes, endothelial cells, and basement membrane. The basement membrane may function as a filtration barrier for molecular entry or spillover, a scaffold to maintain vascular morphology, and a structure to prevent pathological vascular proliferation. The function of the pericytes is contractile and phagocytic, regulating blood flow through this region of the capillary bed. Endothelial cells function to synthesize and secrete a variety of endocrine substances. When glucose levels are elevated, the proliferation rate of retinal microvascular pericytes is reduced, and extensive pericyte death can cause loss of regional retinal blood flow regulation and disrupt capillary integrity. Another phenomenon in diabetic retinopathy is the thickening of the capillary basement membrane, the mechanism of which is uncertain. The replication of endothelial cells is delayed and cell death is accelerated in the hyperglycemic environment. The mechanism of microvascular damage in hyperglycemic state is not well understood. Hyperglycemia stimulates the hardening of plasma proteins, causing the accumulation of red blood cells and platelets, and the thickening of capillary basement membrane, resulting in a series of biochemical or pathophysiological changes caused by reduced capillary perfusion, retinal anemia, increased tissue oxygen demand, reduced oxygen supply, and increased production of some harmful metabolites. Fifth, the increase of endothelin makes a large number of neovascularization. Endothelin is the most powerful and longest lasting vasoconstrictor known. Under physiological conditions, the level of endothelin in blood is very low; under pathological conditions such as ischemia and hypoxia, the abnormal expression and release of endothelin is an important link in the development of certain diseases. Elevated blood glucose inhibits endothelin release, reduces vasoconstrictor activity, decreases oxygen delivery, and hypoxia leads to retinal microvascular dilation. With the prolongation of the disease, the formation of advanced glycosylation end products, thickening of the microvascular basement membrane, and increasingly severe endothelial cell damage are factors that stimulate the elevation of plasma and local endothelin. Endothelin, by strongly constricting blood vessels and promoting the proliferation of smooth muscle cells and endothelial cells, causes serious impairment of retinal microcirculation, narrowing of small arteries and veins, increased capillary fragility and permeability, causing hemorrhage and exudative lesions; in addition, capillary occlusion, aggravating retinal ischemia and hypoxia, stimulating the release of vascular growth factor and producing a large number of neovascularization without cell structure. Sixth, the increase of vascular factor makes the harm of neovascularization aggravated. Vascular factors are a multifunctional class of potent cell growth regulators, and the retina has many vascular endothelial cell proliferation factors and proliferation inhibition factors. Under normal conditions, there is a dynamic balance between vascular proliferative factors and inhibitory factors. When the activation and/or production of vasoproliferative factors increases, or the number and/or activity of inhibitory factors decreases, this balance is disturbed and neovascularization occurs. Retinal ischemia is the underlying abnormality that causes retinopathy to enter the proliferative phase. Two factors are required for the development of retinal neovascularization: first, inflammation and its products, a hypoxic retina or a specific growth factor; and second, the presence of diseased retinal vessels for its induction. In the physiological case, the retinal vessels do not invade the vitreous due to the presence of inhibitory factors. In the pathological case, neovascularization can cause extensive damage to a variety of tissue components in the eye, to the point that neovascularization has become the leading cause of disease worldwide. In conclusion, the pathogenesis of diabetic retinopathy is a very complex pathological process. It may be the result of a multifactorial and multistage action. It is generally accepted that hyperglycemia lasting several years is a prerequisite for the development of diabetic retinopathy. There is metabolic damage first, followed by microvascular damage. Under the stimulation of hyperglycemia, cellular Na-K-ATPase activity is affected by interfering with inositol metabolism and the formation of late glycosylation end product products. It increases capillary permeability, thickens the basement membrane, aggravates the accumulation of late glycosylation end products, narrows capillary lumen, retinal ischemia, releases vasoproliferative factors, promotes neovascularization, and develops proliferative diabetic retinopathy.