Proposed summary of cellular mechanisms of renal protection with postischemic isoflurane treatment. Collectively, our data suggest that anesthesia with isoflurane increases interleukin (IL)-11 messenger RNA and protein synthesis via transforming growth factor-β1 (TGF-β1) signaling. We propose that IL-11 synthesized subsequently activates interleukin-11 receptor (IL-11R) in neighboring renal tubules or endothelial cells to induce cytoprotective signaling. Because previous studies have shown that IL-11 reduces the activity of a well-known proinflammatory transcription factor NF-kB,^49,50  it is highly possible that IL-11 generated with isoflurane treatment may also attenuate NF-kB activity to protect against renal inflammation and injury after acute kidney injury. SMADs are intracellular proteins that transduce extracellular signals from TGF-β1 to the nucleus to initiate downstream gene transcription. Hypothetical pathways (e.g., NF-kB inhibition) leading to cytoprotection are shown in dashed lines. We previously showed that IL-11 produces renal protection by direct induction of sphingosine kinase-1 via nuclear translocation of hypoxia-inducible factor (HIF)-1α.¹⁴  IR = ischemia reperfusion; NF-kB = nuclear factor κ-light-chain-enhancer of activated B cells; PS = phosphatidylserine; SMAD = SMA (from Caenorhabditis elegans protein sma for small body size) and MAD (from Drosophila protein mothers against decapentaplegic) related family of transduction proteins.