ArticleMolecular biology reports2026
The effects of netarsudil ophthalmic solution on the expression of genes involved in fibrogenesis in orbital fibroblasts of patients with thyroid eye disease.
Article in Molecular biology reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThyroid eye disease (TED) is an autoimmune orbital disorder characterized by fibroblast activation, myofibroblast differentiation, and excessive extracellular matrix production. RhoA/ROCK signaling is increasingly implicated in these fibrotic processes. This study aimed to investigate the effects of the Rho-associated protein kinase (ROCK) inhibitor netarsudil on the expression of fibrogenesis-related genes in orbital fibroblasts derived from patients with TED. METHODS AND
resultsPrimary orbital fibroblasts were isolated from two patients with TED. Cells were treated with varying concentrations of netarsudil (ranging from 2 × 10
conclusionsOur findings suggest that non-cytotoxic dose of netarsudil, is insufficient to reverse the constitutively pro-fibrotic transcriptional program in TED orbital fibroblasts. The lack of direct antifibrotic efficacy highlights the complexity of TED fibrogenesis and suggests that redundant or parallel signaling pathways may limit the impact of isolated ROCK inhibition. Further research is required to evaluate combination therapies or alternative targets in TED-related fibrosis.
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