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Model of how ER stress, MAPK pathways, and SRA engagement conspire to induce apoptosis in FC-loaded macrophages. Excess FC loading of the ER induces an ER stress response that leads to activation of p38 and JNK. Activation of p38, in turn, induces the UPR effector, CHOP. Three pathways—p38-CHOP, JNK, and engagement of the SRA—combine to induce apoptosis. Ac-LDL is able to trigger all three pathways, because it delivers cholesterol to the cells and is a ligand for the SRA.
