Figure 4.

Schematic diagrams of diverging and converging mechanisms underlying the tissue protection and repair effects of medical gases. Biological gases (top left), in general, effect via modulating HO1/HSP/L‐type Ca²⁺ channels, NOS, sGC, PI3K/Akt, MEK, and PGC1α to regulate gene expressions of CREB/mTOR, growth factors, and HIF‐1α/VEGF. Also involved are TLRs that affect p38 MAPK and NF‐κB to impede proinflammatory cytokines, as well as ROS and GSK‐3β to modulate mPTP/cytochrome c and Bax/Bcl2/caspases. Conversely, noble gases (top right) work by agonizing GABA_A receptors and antagonizing NMDA receptors, ROS, and mPTP/mitochondrial K⁺ channels to ameliorate excitotoxicity, caspase activation, and cell death. More specifics can be found in the text regarding the signaling pathways of each gas (note: definitions of abbreviations and acronyms are listed in Sections S3 and S4: Supporting Information).