The interface targeting hnRNPA2B1 regulates the repression of transthyretin against human retinal microvascular endothelial cells in high glucose environment.

This work suggests that the formation of the TTR-hnRNPA2B1 complex plays vital roles in hyperglycemia, and modification of this interface regulates the TTR-mediated inhibition of hREC neovascularization via the STAT-4/miR-223-3p/FBXW7 pathway. This mechanism could have important implications for diabetic retinopathy treatment.