Figure 8.

Role of eEF1A-1 in palmitate-induced cell death. Under conditions of FA overload in nonadipose tissues, the cellular capacity to store FAs as triglycerides or to use FAs for energy is overwhelmed. This FFA overload can lead to the production of ROS, which can, in turn, induce ER stress. Prolonged or severe ER stress, which may occur in the presence of excess palmitate, can lead to further ROS accumulation, potentially amplifying the apoptotic/cell death response. Palmitoyl CoA, generated by esterification of palmitate as it enters the cell, may also induce ER stress directly, leading to the production and accumulation of ROS and subsequent apoptosis/cell death. In either of these scenarios, eEF1A-1 mediates actin cytoskeleton changes involved in the progression of the lipotoxic cell death response downstream of induction of oxidative and ER stress.