Deletion of toll-like receptor 4 ameliorates diabetic retinopathy in mice

Background Diabetic retinopathy is a common and specific microvascular complication of diabetes, which is also the leading cause of preventable blindness. Therefore, we aimed to find a promising therapeutic strategy for diabetic retinopathy. Methods To investigate the role of toll-like receptor 4 (TLR4) in the diabetic retinopathy, we injected streptozotocin (STZ) into wild-type (wt) and TLR4 knock-out mice to induce diabetes. Results While STZ induced diabetes both in wt and TLR4(-/-) mice, deletion of TLR4 in diabetic mice significantly improved diabetic retinopathy compared to diabetic wt mice, as judged by the enhanced thickness of retinal tissue. Furthermore, TLR4-dependent NF-kappa B pathway, inflammatory cytokine release and the expressions of vascular endothelial growth factor (VEGF) and glial fibrillary acidic protein (GFAP), which were all remarkably stimulated in STZ-injected wt mice, were inhibited in STZ-injected TLR4(-/-) mice. Conclusion TLR4 could serve as an independent target for treating diabetic retinopathy.

Automated summary

This study found that TLR4 can serve as an independent target for treating diabetic retinopathy, and the absence of TLR4 can significantly improve the manifestations of diabetic retinopathy.