Abstract:

Thhe endoplasmic reticulum (ER) is the principal site for the synthesis, folding and maturation of most secreted proteins in the cell and essential for most cellular activities. Conditions that impair the folding capacity of the ER cause ER stress and induce a set of signaling pathways termed the unfolded protein response (UPR). If the protective mechanism activated by the UPR is not sufficient to restore normal ER function, cells die by apoptosis mechanism. Recent research suggests that ER stress and UPR play important roles in the metabolic disorders such as diabetes and obesity, cancer, immune response and in some neurodegenerative diseases such as Alzheimer, Parkinson, Huntington. Further studies on ER stress and UPR are necessary to clarify the exact role of this physiological mechanism and provide novel avenues to potential therapies. This review will provide an overview of ER stress, the UPR signaling pathways and ER stress induced apoptosis mechanism.

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