Endoplasmic reticulum stress: cell life and death decisions.
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.
Xu
Chunyan
C
The Burnham Institute for Medical Research, La Jolla, California 92037, USA.
Bailly-Maitre
Beatrice
B
Reed
John C
JC
D000818:Animals; D016923:Cell Death / Q000187:drug effects; D003920:Diabetes Mellitus / Q000188:drug therapy / Q000378:metabolism*; D004721:Endoplasmic Reticulum / Q000378:metabolism*; D006801:Humans; D000860:Hypoxia / Q000188:drug therapy / Q000378:metabolism*; D015428:Myocardial Reperfusion Injury / Q000188:drug therapy / Q000378:metabolism*; D019636:Neurodegenerative Diseases / Q000188:drug therapy / Q000378:metabolism*; D015398:Signal Transduction / Q000187:drug effects; D013312:Stress, Physiological / Q000378:metabolism