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The **choroidal vasculature** refers collectively to the network of blood vessels within the **choroid**, which is part of the uvea—the middle layer of tissue in the wall of the eye. This highly vascularized structure lies between the retina and sclera. Its primary function is supplying oxygen and nutrients to the outer layers of the retina, including photoreceptors critical for vision. The system includes several distinct layers: Haller’s layer (large vessels), Sattler’s layer (medium-sized vessels), and most importantly for retinal support, a dense capillary bed called **the choriocapillaris** adjacent to Bruch’s membrane. The segmental nature of its arterial supply means that localized blockages can have significant clinical consequences for vision. Abnormalities or dysfunctions in this vascular network play key roles in ocular diseases such as age-related macular degeneration and central serous chorioretinopathy[1][4][5][6]. However, "choroidal vasculature" is an anatomical structure rather than a discrete molecular target; thus it does not fit standard definitions used for therapeutic targets like receptors or enzymes. Drugs such as anti–VEGF agents—bevacizumab, ranibizumab, aflibercept—target pathological processes involving abnormal growth in the choroidal vasculature but do not directly target "choroidal vasculature" as a molecular entity. Imaging biomarkers such as subfoveal choroidal thickness, choroidal vascularity index are used for disease monitoring but are not molecular biomarkers per se. Therapeutic challenges relate more to drug delivery and off-target effects when treating diseases affecting this tissue; e.g., intraocular inflammation with some anti–VEGF agents. There is something incorrect about using "Choroidal vasculature" as a therapeutic target name—it refers broadly to an anatomical network rather than any specific molecule/protein/receptor/enzyme typically considered druggable targets. Drugs may act on processes affecting these vessels but do not bind/interact with “choroidal vasculature” itself at a molecular level.
Anti–VEGF drugs inhibit vascular endothelial growth factor signaling to reduce abnormal vessel proliferation and leakage in diseases like polypoidal choroidal vasculopathy and neovascular AMD
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