A study published online as part of ARVO’s 2020 collection suggests that treatment with the rho-kinase (ROCK) inhibitor ripasudil may suppress the expression of genes responsible for abnormal extracellular matrix deposition and guttae formation in Fuchs’ endothelial corneal dystrophy (FECD).
Researchers took endothelial cell–Descemet’s membrane (EDM) complexes from FECD patients during Descemet’s membrane endothelial keratoplasty surgery and from normal donor corneas unsuitable for transplantation. The team analyzed gene and protein expression with and without a single dose of 30µM ripasudil.
The researchers found the ROCK inhibitor caused significant downregulation of FECD-specific genes such as agrin, fibronectin, collagen type I and collagen type III, as well as alpha-smooth muscle actin—both on the mRNA and protein level—compared with untreated controls. They noted that suppressive effects were more pronounced in FECD specimens than in normal control specimens and were maintained for up to 72 hours of incubation. They observed discrete changes in the expression levels of a number of components of the signaling pathways upon treatment with ripasudil.
The study authors conclude that this approach could serve as a novel anti-fibrotic treatment in patients with early-stage FECD.
Kruse FE, Zenkel M, Tourtas T, et al. Inhibition of the Rho-ROCK pathway modulates abnormal matrix production in Fuchs’ corneal endothelial dystrophy. ARVO 2020. Abstract #1182.