NSC23766 effectively inhibited retinal neovascularization by disrupting the positive feedback loop between Rac1 and VEGFR2.

ABSTRACT: Retinal neovascularization (RNV) is a leading cause of blindness. Although anti-VEGF therapy remains the first-line treatment for RNV, a subset of patients exhibits poor or no response to anti-VEGF agents. Therefore, exploring alternative therapeutic strategies is imperative. Rac1, a small GTPase, has been reported to regulate angiogenesis through multiple signaling pathways. Nevertheless, the precise role of Rac1 in RNV progression remains unclear. Our study demonstrates that NSC23766, a Rac1 activation inhibitor, effectively attenuates VEGF-induced angiogenic responses in human retinal microvascular endothelial cells (HRMECs), including proliferation, migration, invasion, and tube formation. Furthermore, phalloidin staining revealed that NSC23766 significantly inhibits VEGF-induced cytos

SUBMITTER: Tang J 

PROVIDER: S-EPMC12635336 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature