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Diabetic retinopathy is one of the major causes of visual impairment and blindness in adult population. The pathology is complex, the metabolic changes induced by the hyperglycemic environment leading to neurodegeneration, microvascular damage, with secondary ischemic and inflammatory changes in the retina. This review aims to update the literature data related to the role of inflammation in the onset and progression of diabetic retinopathy. Thus, the molecular and biochemical mechanisms triggered by excess glucose increase the expression of genes involved in inflammatory processes, which leads to the synthesis of inflammatory cytokines such as Il1, Il6, TNF alpha as well as complement activation. Furthermore, recent evidence has demonstrated that both systemic and ocular prolonged inflammation are correlated with the progression of diabetic retinopathy. In conclusion, preventing and/or reducing the progression of diabetic retinopathy requires both rigorous glycemic control in diabetic patients and targeted interference of the specific inflammatory pathways involved. [ABSTRACT FROM AUTHOR]

Age-related macular degeneration (AMD) is a complex, chronic, and progressive disease which affects the macular area, being one of the leading causes of irreversible vision loss worldwide. Specific alterations of retinal structure occur at the macular level, which regarding its severity can range from the presence of drusen to the development of geographic atrophy or choroidal neovascularization. AMD has long been considered a degenerative disease, but new studies highlight the role of inflammation present both in the atrophic form and in the exudative form. The present review is based on comprehensive research on PubMed and Web of Science databases, and it aims to describe the inflammatory pathways involved in AMD onset and progression. Understanding the molecules involved in AMD pathogenesis, and their mechanism of action, is crucial because they can be both biomarkers with a predictive role in disease management, as well as potential therapeutic targets. [ABSTRACT FROM AUTHOR]