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The collagen-hyaluronan network is the primary structural component of the vitreous body, a clear, gel-like substance filling the posterior segment of the eye (Sebag J, 1989, The Vitreous: Structure, Function, and Pathobiology). This complex consists of a scaffold of fine collagen fibrils, predominantly Type II, interspersed with high-molecular-weight hyaluronan molecules that provide volume and viscoelasticity (Bishop PN, 2000, Progress in Retinal and Eye Research). Its biological function is to maintain the eye's shape, provide shock absorption, and ensure optical transparency for light to reach the retina. In various ocular pathologies, such as vitreomacular traction (VMT) or macular holes, the network fails to detach properly from the retinal surface, leading to mechanical stress and vision loss (Gandorfer A, et al., 2012, NEJM). Therapeutic intervention, known as pharmacologic vitreolysis, utilizes enzymes like ocriplasmin to degrade the proteinaceous links within this network or at the vitreoretinal interface. By inducing vitreous liquefaction and posterior vitreous detachment, these drugs alleviate tractional forces without the need for invasive surgery (Stalmans P, et al., 2012, NEJM).
Enzymatic degradation of structural proteins (collagen, laminin, fibronectin) or glycosaminoglycans (hyaluronan) to promote vitreous liquefaction (synchysis) and separation from the retina (syneresis).
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