Glucocorticoids are widely used as an ophthalmic medication. A common, sight-threatening adverse event of glucocorticoid usage is ocular hypertension, caused by dysfunction of the conventional outflow pathway. We report that netarsudil, a rho-kinase inhibitor, decreased glucocorticoid-induced ocular hypertension in patients whose intraocular pressures were poorly controlled by standard medications. Mechanistic studies in our established mouse model of glucocorticoid-induced ocular hypertension show that netarsudil both prevented and reduced intraocular pressure elevation. Further, netarsudil attenuated characteristic steroid-induced pathologies as assessed by quantification of outflow function and tissue stiffness, and morphological and immunohistochemical indicators of tissue fibrosis. Thus, rho-kinase inhibitors act directly on conventional outflow cells to prevent or attenuate fibrotic disease processes in glucocorticoid-induced ocular hypertension in an immune-privileged environment. Moreover, these data motivate the need for a randomized prospective clinical study to determine whether netarsudil is indeed superior to first-line anti-glaucoma drugs in lowering steroid-induced ocular hypertension.© 2021, Li et al.
About The Author
Guorong Li,Chanyoung Lee,A Thomas Read,Ke Wang,Jungmin Ha,Megan Kuhn,Iris Navarro,Jenny Cui,Katherine Young,Rahul Gorijavolu,Todd Sulchek,Casey Kopczynski,Sina Farsiu,John Samples,Pratap Challa,C Ross Ethier,W Daniel Stamer
A Thomas Read
C Ross Ethier
W Daniel Stamer