Rock inhibitors to treat diabetic retinopathy

In diabetic retinopathy, the exact mechanisms leading to retinal capillary closure and to retinal barriers breakdown remain imperfectly understood. Rho-associated kinase (ROCK), an effector of the small GTPase Rho, involved in cytoskeleton dynamic regulation and cell polarity is activated by hyperglycemia. In both GK rat and in human type 2 diabetic retinas, ROCK-1 is activated and associated with non-apoptotic membrane blebbing in retinal vessels and in retinal pigment epithelium (RPE) that respectively form the inner and the outer barriers. Activation of ROCK-1 induces focal vascular constrictions, endoluminal blebbing and subsequent retinal hypoxia. In RPE cells, actin cytoskeleton remodeling and membrane blebs in RPE cells contributes to outer barrier breakdown. Diabetes-induced cell blebbing may contribute to ischemic maculopathy and represent an intervention target. The present invention relates to methods and pharmaceutical compositions for the treatment of retinal capillary non-perfusion. In particular, the present invention relates to a method of treating retinal capillary non-perfusion in a subject in need thereof comprising administering to the subject a therapeutically effective amount of a ROCK inhibitor.

Keywords: Diabetic Retinopathy - Drug repositionning - ROCK inhibitor-Fasudil
Inventors:
Francine BEHAR-COHENPatricia CRISANTI-LASSIAZ
Publications:
Sci Rep. 2017 Aug 18;7(1):8834. doi: 10.1038/s41598-017-07329-y.

Reference:

BIO15371-T1

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