Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on imrpress.com as a courtesy and upon agreement with Frontiers in Bioscience.
Academic Editor: Catherine Brenner
The ndoplasmic reticulum (ER) function is critical for multiple cellular activities. Hence, impairment of the physiological function of the ER, such as accumulation of unfolded proteins or disturbance of lumenal calcium homeostasis, leads to an evolutionarily conserved adaptive response known as the ER stress response. Activation of this self-protective pathway gives the cell a chance to restore normal ER function. In the case of prolonged or severe stress conditions, or if the ER dysfunctions cannot be compensated, apoptosis is ultimately activated to eliminate stressed cells. Although the molecular mechanisms involved in ER stress-mediated apoptosis are poorly understood, it is known that ER and mitochondria can cooperate to induce cell death. In this review, we discuss the commitment and development of the lethal crosstalk between ER and mitochondria and focus on the role of the mitochondrial permeability transition pore complex in these processes.