Abstract
Chen et al. demonstrate endothelial expression of Toll-like receptor 4 (TLR4) in the outer medulla of the kidney early in the course of ischemic acute kidney injury. Furthermore, they provide data that support the hypothesis that activation of endothelial TLR4 in the early extension phase of AKI by damage-associated molecular pattern molecules released from injured tubules results in endothelial activation. This activation can serve to amplify inflammation and tubular damage.