APA
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Li, G., Lee, C., Read, A., Wang, K., Navarro, I., Cui, J., … Stamer, W. (2021). Anti-fibrotic activity of a rho-kinase inhibitor restores outflow function and intraocular pressure homeostasis. Elife, 10, e60831.
Chicago/Turabian
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Li, Guorong, Chanyoung Lee, A. Read, Ke Wang, I. Navarro, J. Cui, Katherine M. Young, et al. “Anti-Fibrotic Activity of a Rho-Kinase Inhibitor Restores Outflow Function and Intraocular Pressure Homeostasis.” Elife 10 (2021): e60831.
MLA
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Li, Guorong, et al. “Anti-Fibrotic Activity of a Rho-Kinase Inhibitor Restores Outflow Function and Intraocular Pressure Homeostasis.” Elife, vol. 10, 2021, p. e60831.
BibTeX Click to copy
@article{guorong2021a,
title = {Anti-fibrotic activity of a rho-kinase inhibitor restores outflow function and intraocular pressure homeostasis},
year = {2021},
journal = {Elife},
pages = {e60831},
volume = {10},
author = {Li, Guorong and Lee, Chanyoung and Read, A. and Wang, Ke and Navarro, I. and Cui, J. and Young, Katherine M. and Gorijavolu, Rahul and Sulchek, T. and Kopczynski, C. and Farsiu, Sina and Samples, J. and Challa, P. and Ethier, C. and Stamer, W.}
}
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, rapidly reversed glucocorticoid-induced ocular hypertension in patients whose intraocular pressures were uncontrolled by standard medications. Mechanistic studies in our established mouse model of glucocorticoid-induced ocular hypertension show that netarsudil both prevented and reversed intraocular pressure elevation. Further, netarsudil reversed 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 efficaciously prevent or reverse fibrotic disease processes in glucocorticoid-induced ocular hypertension. These data motivate a novel indication for these agents to prevent or treat ocular hypertension secondary to glucocorticoid administration, and demonstrate the antifibrotic effects of rho-kinase inhibitors in an immune-privileged environment.