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The target refers to the broad array of cellular components, including lipid bilayers and functional proteins, that undergo oxidative damage during photodynamic therapy (PDT) with verteporfin [1, 3]. Verteporfin is a photosensitizing agent that selectively accumulates in neovascular endothelial cells, often mediated by binding to low-density lipoprotein (LDL) receptors [2, 3]. Upon activation by a specific wavelength of red light (689 nm), the drug transfers energy to molecular oxygen, generating highly reactive singlet oxygen and other reactive oxygen species (ROS) [1, 3]. These ROS cause immediate, localized damage to nearby lipids and proteins, resulting in lipid peroxidation and protein denaturation [3]. This process leads to cell death and the subsequent occlusion of abnormal blood vessels, which is the primary therapeutic goal in treating conditions like age-related macular degeneration (AMD) [2, 3]. Additionally, verteporfin is recognized in research for its light-independent ability to inhibit the YAP/TAZ transcriptional co-activators, though its clinical efficacy in ophthalmology is driven by ROS-mediated membrane damage [4].
Generation of singlet oxygen and reactive oxygen species (ROS) upon light activation, leading to localized lipid peroxidation and protein oxidation [1, 3].
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