Link to bioRxiv paper: http://biorxiv.org/cgi/content/short/2020.07.17.208207v1?rss=1 Authors: Li, G., Lee, C., Read, A. T., Wang, K., Navarro, I., Cui, J., Young, K., Gorijavolu, R., Sulchek, T., Kopczynski, C., Farsiu, S., Samples, J., Challa, P., Ethier, C. R., Stamer, W. D. Abstract: 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. Copy rights belong to original authors. Visit the link for more info