Relationship between Oxidative Stress, Circadian Rhythms, and AMD

Figure 2

Development of AMD. AMD is mainly due to photochemical damage and oxidative stress. In the figure, the progression of AMD is represented by the cellular structure of the normal macula (left side), the dry AMD (center), and the wet AMD (right side). In the left side of the image, the cells in the macula are normal. In the dry form of AMD (center), drusen impair the metabolic connection between the choroid and the upper layers of macula, leading to the degeneration of the RPE and photoreceptors. In the wet form of AMD (right side), the production of neovascular factors results in the formation of choroidal neovascularization (CNV) with subsequent fluid leakage and major degeneration of the RPE and photoreceptors. In the normal ageing process, lipids accumulate in Bruch’s membrane, causing the membrane to thicken and improving the oxidative distress. Moreover, Bruch’s membrane lacks an adequate intrinsic antioxidant system. Furthermore, the lipids can bind the macrophages, inducing the secretion of vascular endothelial growth factor (VEGF). The production of inflammatory factors improves the damage to the RPE and photoreceptors and induces the formation of functional microvascular networks (choroidal neovascularization). Antioxidant factors might prevent the disease and delay its progression. In the upper portion of the image, the pool of nutrients involved in the onset (left side) and progression (right side) of AMD are listed. From Zampatti et al. [131], with the permission of the authors and Elsevier. Rightlinks License number is 3679500345328.