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The **trabecular meshwork** is a specialized spongy tissue located at the angle between the cornea and iris in the anterior chamber of the eye. It serves as the primary drainage route for aqueous humor—the clear fluid that nourishes avascular structures such as the lens and cornea—by channeling it from the anterior chamber into Schlemm’s canal and then into systemic circulation. This process is essential for maintaining normal intraocular pressure (IOP). Dysfunction or blockage within this structure leads to elevated IOP, which can damage the optic nerve and result in vision loss characteristic of glaucomatous diseases. The trabecular meshwork consists of three main layers—uveal meshwork, corneoscleral meshwork, and juxtacanalicular tissue—with each contributing differently to resistance against fluid outflow. Most current therapies for open-angle glaucoma aim either to increase aqueous humor drainage through this pathway or reduce its production; newer drug classes such as Rho kinase inhibitors specifically target cellular mechanisms within this tissue to enhance fluid egress.[1][3][6] **Note:** The "trabecular meshwork" is not a molecular therapeutic target like a receptor or enzyme but rather an anatomical/structural target relevant in ophthalmology. Therefore, *is_target* should be set **false**, *is_incorrect* should be set **true**, since it does not fit standard definitions for molecular drug targets such as receptors or enzymes.[1][3]
Increase aqueous humor outflow through relaxation or remodeling of trabecular meshwork cells and extracellular matrix[2][4] - Rho kinase inhibitors relax TM cells by disrupting actin stress fibers and increasing intercellular space[2] - Muscarinic agonists like pilocarpine contract ciliary muscle to widen TM spaces and enhance outflow[4]
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