Cytoskeletal involvement in the regulation of aqueous humor outflow.

Fluid flow in the anterior chamber maintains intraocular pressure (IOP) and globe shape and supplies oxygen and nutrients to the nonvascularized cornea, lens, and trabecular meshwork (TM). Glaucoma is a progressive optic neuropathy often caused by elevated IOP consequent to abnormally high resistance to aqueous humor drainage via the TM and Schlemm’s canal. Compounds with cytoskeletal effects offer therapeutic possibilities for substantial long-term IOP reduction. Most current IOP-reducing agents either suppress aqueous humor production or increase outflow through the ciliary muscle, thus reducing aqueous humor flow through the TM, perhaps compromising an already compromised tissue and potentially stressing the cornea and lens. Glaucoma patients usually receive several of these agents concurrently. Recent studies indicate that the TM cytoskeleton may be involved in the regulation of aqueous humor outflow. A cytoskeletal agent acting directly on the TM/Schlemm’s canal to reduce outflow resistance would be more consistent with normal physiological function, and recent developments indicate that this approach is moving toward fruition.