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Retinal vascular permeability is a physiological process and pathological hallmark characterized by the leakage of fluid, plasma proteins, and lipids from retinal capillaries into the surrounding neural tissue (Campochiaro, 2015, PMID: 25134421). This phenomenon occurs due to the breakdown of the blood-retinal barrier (BRB), which is composed of non-fenestrated endothelial cells with tight junctions, pericytes, and glial cells (Antonetti et al., 2021, PMID: 33461561). In diseases such as diabetic retinopathy and neovascular age-related macular degeneration, the upregulation of pro-permeability factors—most notably Vascular Endothelial Growth Factor (VEGF)—disrupts these tight junctions, leading to macular edema and significant visual impairment (PubMed, PMID: 11029558). While retinal vascular permeability is a clinical endpoint rather than a single molecular target, it is the primary focus of therapeutic intervention in retinal vascular diseases. Current pharmacological strategies involve the use of intravitreal anti-VEGF agents, such as aflibercept and ranibizumab, which sequester VEGF to stabilize the vasculature and reduce leakage (FDA, 2023). Monitoring this process via imaging techniques like optical coherence tomography is essential for managing retinal vascular diseases and evaluating the efficacy of anti-angiogenic therapies (PubMed, PMID: 30130518).
Inhibition of pro-permeability signaling molecules, primarily Vascular Endothelial Growth Factor (VEGF) and Angiopoietin-2 (Ang-2), to restore the integrity of the blood-retinal barrier (Campochiaro, 2015, PMID: 25134421).
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