Open Access
Article
Role of the permeability transition pore complex in lethal inter-organelle crosstalk
Ossama Sharaf El Dein1,Cindy Gallerne1,Aurelien Deniaud1,Catherine Brenner1,Christophe Lemaire1
1
Universite de Versailles/SQY, PRES UniverSud Paris, CNRS UMR 8159, 45 avenue des Etats-Unis, 78035 Versailles, France
DOI: 10.2741/3465 Volume 14 Issue 9, pp.3465-3482
Published: 01 January 2009
(This article belongs to the Special Issue Apoptosis and mitochondria)
Abstract

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.

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Ossama Sharaf El Dein, Cindy Gallerne, Aurelien Deniaud, Catherine Brenner, Christophe Lemaire. Role of the permeability transition pore complex in lethal inter-organelle crosstalk. Frontiers in Bioscience-Landmark. 2009. 14(9); 3465-3482.