Figure 3
From: The Hepatic Response to Thermal Injury: Is the Liver Important for Postburn Outcomes?
Schematic of suggested pathways involved in the hepatic response postburn. Thermal injury leads to gross alterations in ER calcium with increased cytosolic calcium concentration. Increased cytosolic calcium induces mitochondrial damage which releases cytochrome c. Cytochrome c increases the existing ER stress/UPR but also binds to the IP3R augmenting the depletion of ER calcium stores. ER stress/UPR leads to cell apoptosis and activation of JNK which phosphorylates the 612 serine of IRS-1, which blocks phosphorylation of tyrosine IRS-1. ER stress/UPR also impairs the prosurvival PI3K/Akt signaling which results in an increased activation of the IP3R increasing ER stress/UPR.