Fig. 10.
Putative molecular mechanism for xenon-mediated protection against remote lung injury. Proposed molecular mechanisms for xenon-mediated protection against remote lung injury due to renal graft ischemia–reperfusion injury (IRI). Xenon activated phosphatidylinositol 3 kinase (PI3K)-Akt-mammalian target of rapamycin (mTOR)-hypoxia-inducible factor (HIF)-1α, leading to enhanced cell survival and proliferation in lung, which prevented high-mobility group protein-1 (HMGB-1) translocation from nuclei to cytoplasm due to damage by oxidative and inflammatory stress, caused by distant renal graft IRI. The pulmonary inflammation and injury were attenuated by xenon treatment. NF-κB = nuclear factor κB; TLR-4 = Toll-like receptor-4; Xe = xenon.