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The internal limiting membrane (ILM) is a specialized basement membrane that forms the interface between the retina and the vitreous body. It is primarily composed of extracellular matrix (ECM) proteins such as collagen type IV, laminin, fibronectin, and various proteoglycans like agrin (Halfter et al., 2008). Biologically, the ILM provides structural support to the retina and serves as a scaffold for the end-feet of Müller glial cells (Ponsioen et al., 2008). In pathological states, such as vitreomacular traction (VMT) or macular holes, the ILM can exert mechanical forces that distort retinal architecture (Gandorfer et al., 2004). Therapeutic strategies targeting the ILM involve either surgical peeling or pharmacological vitreolysis using proteolytic enzymes. Ocriplasmin, a recombinant protease, targets laminin and fibronectin to facilitate the separation of the vitreous from the retina (Stalmans et al., 2012). This pharmacological approach aims to resolve vitreomacular adhesion without the need for invasive surgery, though it requires precision to avoid damaging the underlying retinal layers (Stalmans et al., 2012).
Proteolytic degradation of extracellular matrix components, specifically laminin and fibronectin, to induce posterior vitreous detachment and resolve vitreomacular adhesion (Stalmans et al., 2012).
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