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Abstract
Disturbances in the normal functions of the ER lead to an evolutionarily conserved
cell stress response, the unfolded protein response, which is aimed initially at compensating
for damage but can eventually trigger cell death if ER dysfunction is severe or prolonged.
The mechanisms by which ER stress leads to cell death remain enigmatic, with multiple
potential participants described but little clarity about which specific death effectors
dominate in particular cellular contexts. Important roles for ER-initiated cell death
pathways have been recognized for several diseases, including hypoxia, ischemia/reperfusion
injury, neurodegeneration, heart disease, and diabetes.