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Schlemm's canal is a circular, endothelium-lined vessel located at the corneoscleral junction (limbus) of the eye, also known as the scleral venous sinus[1][5]. It is not a single molecule, receptor, or conventional therapeutic target, but rather an anatomical and functional structure that acts as the main drainage pathway for aqueous humor from the anterior chamber into the episcleral veins, thus regulating intraocular pressure[1][5][8]. This vessel exhibits features of both blood and lymphatic endothelium, expressing markers such as PROX1 and VEGFR3, but lacks others (e.g., LYVE-1)[1][4][9]. Schlemm's canal is essential in the pathophysiology of glaucoma, as increased resistance or obstruction can elevate intraocular pressure leading to optic nerve damage[3][5][8]. Although it is sometimes the focus of surgical or gene therapy interventions for glaucoma, it is not a protein, receptor, or gene product and does not have drug interactions in the sense of typical molecular targets[3][7]. Markers such as PROX1, VE-cadherin, and VEGFR3 are studied for their roles in canal development, function, and as potential biosensors for monitoring canal integrity in disease[7]. Dysfunction or developmental absence of Schlemm's canal results in fluid imbalance and is directly linked to glaucoma[1][3][7].
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