Figure 7
From: Osteopontin deficiency aggravates hepatic injury induced by ischemia–reperfusion in mice
Schematic representation showing the potential roles of OPN in hepatic I–R injury. The hepatic I–R with 45 min of ischemia followed by 4 h of reperfusion induced upregulation of OPN and revealed its protective role in I–R injury. Endogenous OPN in hepatocytes conferred partial resistance to cell death induced by OGD and TNFα. This could be mediated by the regulation of the Bcl2 and ATP levels by OPN. Endogenous OPN in macrophages also mediated negative feedback on iNOS-derived NO production and partially limited liver macrophage activation and TNFα production in response to an inflammatory signal. The decreased rate of death of hepatocytes could consequently decrease the activation of liver macrophages and thus macrophage-mediated NO and TNFα release. Finally, lowering TNFα and NO levels could prevent additional hepatocyte injury induced by inflammation
