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Choroidal neovascular endothelium refers to the specialized layer of endothelial cells that form abnormal, leaky blood vessels originating from the choroid and extending into the subretinal space [1][6]. This pathological process, known as choroidal neovascularization (CNV), is the hallmark of neovascular age-related macular degeneration (nAMD) and is a leading cause of severe vision loss [1][10]. These endothelial cells are characterized by high sensitivity to pro-angiogenic factors, particularly vascular endothelial growth factor (VEGF), which drives their proliferation, migration, and increased vascular permeability [2][14]. Therapeutic strategies primarily focus on neutralizing VEGF or its receptors to inhibit vessel growth and reduce fluid leakage [1][17]. Additionally, photodynamic therapy (PDT) uses light-activated drugs like verteporfin to selectively damage these cells [9][10]. While not a single molecule, the CNV endothelium serves as a critical cellular target for a wide range of biologics and small molecules aimed at preserving retinal architecture and visual function [6][13].
Inhibition of VEGF-A signaling, inhibition of Ang-2, and photoactivation-induced cytotoxicity [1][2][10].
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