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Updated: Jul 1, 2026

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye
Published on: June 20, 2015
The role of the actomyosin system in regulating trabecular fluid outflow
Baohe Tian1, B'Ann T Gabelt, Benjamin Geiger
1Department of Ophthalmology & Visual Sciences, University of Wisconsin, Madison, WI 53792-3220, USA.
Abstract:
Abnormally high resistance to aqueous humor drainage via the trabecular meshwork and Schlemm's canal is highly correlated with the development of primary open-angle glaucoma. Contractility of the actomyosin system in the trabecular cells or inner wall endothelium of Schlemm's canal is an important factor in the regulation of outflow resistance. Cytoskeletal agents, affecting F-actin integrity or actomyosin contractility, or gene therapies, employing overexpression of caldesmon or Rho-A inhibition, can decrease outflow resistance in the drainage pathway. In this review, we discuss the mechanisms underlying these and similar effects on trabecular outflow resistance in living animals and/or in cultured ocular anterior segments from enucleated animal or human eyes.
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