What is it about?
Retinopathy of prematurity (ROP) has become a more frequently seen clinical condition with the increasing survival of very immature infants. However, the current treatments for ROP, like anti-VEGF agents and laser treatment, have potential side effects or are hard to be performed on neonates. Our study was to explore a new mechanism that might work in the progress of the disease. By using cultured human retinal microvascular endothelial cells and the mouse model of ROP, we revealed that TLR4 activated MAP4K4 signaling played a critical role in the progress of the ROP. And TAK-242, a small molecular inhibitor of TLR4, not only had an effective therapeutic effect on the mouse model of ROP but also had an additive or synergistic effect with anti-VEGF therapy on the disease. In summary, our research identified new molecular basis and regulatory mechanisms of retina aberrant angiogenesis and provided a potential treatment for ROP.
Featured Image
Read the Original
This page is a summary of: Role of TLR4-MAP4K4 signaling pathway in models of oxygen-induced retinopathy, The FASEB Journal, November 2018, Federation of American Societies For Experimental Biology (FASEB),
DOI: 10.1096/fj.201801086rr.
You can read the full text:
Contributors
The following have contributed to this page







