Abstract
Retinal pigment epithelial (RPE) cells are an essential part of the human eye because they not only mediate and control the transfer of fluids and solutes but also protect the retina against photooxidative damage and renew photoreceptor cells through phagocytosis. However, their function necessitates cumulative exposure to the sun resulting in UV damage, which may lead to the development of age-related macular degeneration (AMD). Several studies have shown that UVB induces direct DNA damage and oxidative stress in RPE cells by increasing ROS and dysregulating endogenous antioxidants. Activation of different signaling pathways connected to inflammation, cell cycle arrest, and intrinsic apoptosis was reported as well. Besides that, essential functions like phagocytosis, osmoregulation, and water permeability of RPE cells were also affected. Although the melanin within RPE cells can act as a photoprotectant, this photoprotection decreases with age. Nevertheless, the changes in lens epithelium-derived growth factor (LEDGF) and autophagic activity or application of bioactive compounds from natural products can reverse the detrimental effect of UVB. Additionally, in vivo studies on the whole retina demonstrated that UVB irradiation induces gene and protein level dysregulation, indicating cellular stress and aberrations in the chromosome level. Morphological changes like retinal depigmentation and drusen formation were noted as well which is similar to the etiology of AMD, suggesting the connection of UVB damage with AMD. Therefore, future studies, which include mechanism studies via in vitro or in vivo and other potential bioactive compounds, should be pursued for a better understanding of the involvement of UVB in AMD.
Highlights
The human eye is a complex structure that allows us to see the world in its many colors, shades, and shapes
The results indicated that UVA was much weaker than UVB in inducing DNA damage and cell death, but after exceeding the tolerable amount of DNA damage, Retinal pigment epithelial (RPE) cells opt to initiate cell apoptosis instead of repairing the DNA damage [47]
UVB could cause damage to the RPE cells via direct DNA damage, oxidative stress, and activation of several different pathways, such as NLRP3, MAPK, P13KAKT, NOTCH, and JAK/STAT, which leads to inflammation, cell apoptosis, and cell death
Summary
The human eye is a complex structure that allows us to see the world in its many colors, shades, and shapes. The human eye mainly consists of three distinct layers: (1) the outer region, made up of the cornea and sclera; (2) the middle layer, consisting of the iris, choroid, and ciliary body; and (3) the inner layer which is the retina These three ocular layers surround three other transparent structures known as the aqueous humor, vitreous humor, and the lens [1]. Wet AMD is characterized by the loss of vision through subchoroidal neovascularization It is through the growth of angiogenic blood vessels that penetrates through Bruch’s membrane and the RPE layer into the subretinal space [9, 10].
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