In a sepsis-induced, myocardial-injured mouse model, molecules H2 promoted protein increase of HO-1, MFN2, and PGC1-1α expression, inhibited sepsis-induced mitochondrial dysfunction, and remodeled fatty acid oxidation in the heart in the sepsis model by increasing myocardial energy [88,89]. The gene discussed is HMOX1; the disease is Sepsis.