Figure 2.

Schematic overview of Helium-induced cardioprotection: this diagram presents a summary of the established mechanisms involved in helium-induced cardioprotection, primarily through the RISK pathway, which is closely associated with changes in Caveolin-related processes. Helium is represented by a purple circle (He). Red arrows indicate activation or up-regulation, while squares denote suppression or down-regulation. Intracellularly, these mechanisms converge on the mitochondria, inhibiting the opening of the mitochondrial permeability transition pore (mPTP). Additionally, the potential pathway of “remote conditioning” by helium is illustrated on the left side of the diagram. Unknown and identified factors (potentially Caveolin, transported via exosomes) mediate protection in distant organs and enhance mitochondrial respiration in remote cells. GPCR = G-protein coupled receptor; MEK-1 = mitogen-activated protein kinase-extracellular signal-regulated kinase-1; ERK1/2 = Extracellular signal-regulated kinase 1/2; IP3 = inositol triphosphate-3; DAG = diacylglycerol; PKC-ε = protein kinase C epsilon; GSK3β = glycogen synthase kinase-3beta; PI3K = Phosphatidylinositol-3-kinase; PDK-1 = phosphoinositide-dependent protein kinase-1; PKB = protein kinase B; mTOR = mammalian target of rapamycin; P53 = Tumor protein P53; mPTP mitochondrial permeability transition pore; eNOS = endothelial nitric oxide synthase; NO = nitric oxide; L-NAME = L-NG-nitroarginine methyl ester; PKA = protein kinase A; mKCa = mitochondrial calcium-sensitive potassium channel; ROS = reactive oxygen species; Pi = inorganic phosphate; ATP = adenosine triphosphate; and ADP = adenosine diphosphate.