Schlemm’s canal (SC)

Schlemm’s canal is a circular, endothelium-lined vessel located at the corneoscleral junction of the eye, serving as the principal outflow route for aqueous humor from the anterior chamber to the episcleral veins and ultimately systemic circulation[1][4][7]. It functions analogously to both blood and lymphatic vessels, expressing unique combinations of vascular and lymphatic markers (e.g., PROX1, VEGFR3, CCL21)[10]. Its inner and outer walls exhibit distinct ultrastructure and molecular signatures. Schlemm’s canal’s patency and cellular function are central to maintenance of intraocular pressure; dysfunction increases resistance to fluid outflow, driving pathological elevation of eye pressure and the development/progression of glaucoma, a leading cause of irreversible blindness worldwide[7][10]. Some modern glaucoma therapies are designed to enhance outflow through Schlemm’s canal either pharmacologically (with Rho kinase inhibitors and miotics) or surgically (via trabecular bypass, canaloplasty, stenting, or minimally invasive glaucoma surgeries)[3][6]. Schlemm’s canal cells are a focus of current therapeutic development and targeted delivery approaches[9]. Despite its importance as a target in ophthalmology, Schlemm’s canal is an anatomical tissue target rather than a discrete protein, receptor, or classic molecular entity.

Other names

canal of Schlemmscleral venous sinusscleral canalscleral sinus

Netarsudil: Increases trabecular meshwork outflow and enlarges the inner wall of Schlemm’s canal, reducing intraocular pressure by promoting aqueous humor drainage. Pilocarpine: Contracts the ciliary muscle, transmitting force to the scleral spur and enhancing aqueous humor outflow through the trabecular meshwork and Schlemm’s canal.