, Volume 18, Issue 5, pp 537–546

New directions in ER stress-induced cell death


  • Susan E. Logue
    • Apoptosis Research Centre, NUI Galway
  • Patricia Cleary
    • Apoptosis Research Centre, NUI Galway
  • Svetlana Saveljeva
    • Apoptosis Research Centre, NUI Galway
    • Apoptosis Research Centre, NUI Galway
Original Paper

DOI: 10.1007/s10495-013-0818-6

Cite this article as:
Logue, S.E., Cleary, P., Saveljeva, S. et al. Apoptosis (2013) 18: 537. doi:10.1007/s10495-013-0818-6


Endoplasmic reticulum (ER) stress has been implicated in the pathophysiology of many diseases including heart disease, cancer and neurodegenerative diseases such as Alzheimer’s and Huntington’s. Prolonged or excessive ER stress results in the initiation of signaling pathways resulting in cell death. Over the past decade much research investigating the onset and progression of ER stress-induced cell death has been carried out. Owing to this we now have a better understanding of the signaling pathways leading to ER stress-mediated cell death and have begun to appreciate the importance of ER localized stress sensors, IRE1α, ATF6 and PERK in this process. In this article we provide an overview of the current thinking and concepts concerning the various stages of ER stress-induced cell death, focusing on the role of ER localized proteins in sensing and triggering ER stress-induced death signals with particular emphasis on the contribution of calcium signaling and Bcl-2 family members to the execution phase of this process. We also highlight new and emerging directions in ER stress-induced cell death research particularly the role of microRNAs, ER-mitochondria cross talk and the prospect of mitochondria-independent death signals in ER stress-induced cell death.


Endoplasmic reticulumStressUnfolded protein responseCell death

Copyright information

© Springer Science+Business Media New York 2013