ABSTRACTDiabetic retinopathy (DR) is one of the most prevalent microvascular complications of diabetes and one of the most frequent causes of blindness in active age. Etiopathogenesis behind this important complication is related to several biochemical, hemodynamic and endocrine mechanisms with a preponderant initial role assumed by polyol pathways, increment of growth factors, accumulation of advanced glycation end products (AGE), activation of protein kinase C (PKC), activation of the renin‐angiotensin‐aldosterone system (RAAS), and leukostasis. Chronic and sustained hyperglycemia works as a trigger to the early alterations that culminate in vascular dysfunction. Hypoxia also plays an essential role in disease progression with promotion of neovascularization and vascular dystrophies with vitreous hemorrhages induction. Thus, the accumulation of fluids and protein exudates in ocular cavities leads to an opacity augmentation of the cornea that associated to neurodegeneration results in vision loss, being this a devastating characteristic of the disease final stage. During disease progression, inflammatory molecules are produced and angiogenesis occur. Furthermore, VEGF is overexpre
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