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The Role of Endoplasmic Reticulum Stress in Cell Survival and Death
Benjamin G Spencer1, John W Finnie2
1Flinders Medical Centre, Southern Adelaide Local Health Network, SA Health, Discipline of Anatomy and Pathology, Adelaide Medical School, University of Adelaide, Adelaide, South Australia, Australia.
Abstract:
It is now increasingly recognized that endoplasmic reticulum (ER) stress, which is caused by the accumulation of overproduced or misfolded proteins in this organelle, contributes to the pathogenesis of a diverse range of human diseases. ER stress initiates the unfolded protein response (UPR) in an attempt to restore cellular protein homeostasis and promote cell survival. However, when ER stress is severe or protracted, and uncompensated, the UPR can fail, resulting in cell death, often by apoptosis. ER stress has received relatively little attention in the veterinary literature and the intent of this mini review is to describe the essential features of ER stress and UPR in determining the survival or demise of an affected cell and encourage further study of its role in the pathogenesis of diseases of domestic animal species. The role of ER stress, particularly when chronic and unrelieved, in the pathogenesis of a number of specific diseases is also discussed.
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