Figure 1.

Schematic of proposed mechanisms for renal proximal tubular Toll-like receptor 9 (TLR9)-mediated exacerbation of ischemic acute kidney injury (AKI).

After renal ischemia reperfusion (IR) injury, endogenous TLR9 is activated by TLR9 ligand (presumably mitochondrial deoxyribonucleic acid [DNA] products), and TLR9 activation leads to NFκB-mediated induction of pro-inflammatory chemokines and cytokines and caspase 3/8-mediated renal tubular apoptosis. IκB, inhibitor of κB; MyD88, myeloid differentiation factor 88; NFκB, nuclear factor kappa-light-chain-enhancer of activated B cells.