MAPK8 and hepatitis A virus infection: The mechanism research revealed that autophagy was enhanced in I/R-induced hepatitis, which could be reversed by exogenous H2S. Moreover, exogenous H2S inhibited c-Jun NH2-terminal kinases (JNK) pathway induced by I/R injury through decreasing JNK1 and extracellular signal-regulated kinase (ERK) phosphorylation, while SP600125, a JNK1 inhibitor, strengthened H2S hepatoprotective effects, indicating that autophagy and JNK pathway are involved in the hepatoprotective effect of exogenous H2S in hepatic I/R injury (Cheng et al., 2014).