Biochemistry (Moscow)

, Volume 70, Issue 2, pp 231–239

Programmed cell death via mitochondria: Different modes of dying


DOI: 10.1007/s10541-005-0105-4

Cite this article as:
Bras, M., Queenan, B. & Susin, S.A. Biochemistry (Moscow) (2005) 70: 231. doi:10.1007/s10541-005-0105-4


Programmed cell death (PCD)is a major component of normal development, preservation of tissue homeostasis, and elimination of damaged cells. Many studies have subdivided PCD into the three categories of apoptosis, autophagy, and necrosis based on criteria such as morphological alterations, initiating death signal, or the implication of caspases. However, these classifications fail to address the interplay between the three types of PCD. In this review, we will discuss the central role of the mitochondrion in the integration of the cell death pathways. Mitochondrial alterations such as the release of sequestered apoptogenic proteins, loss of transmembrane potential, production of reactive oxygen species (ROS), disruption of the electron transport chain, and decreases in ATP synthesis have been shown to be involved in, and possibly responsible for, the different manifestations of cell death. Thus, the mitochondria can be viewed as a central regulator of the decision between cellular survival and demise.

Key words

apoptosis ATP autophagy Bcl-2 mitochondria necrosis-like PCD ROS 



apoptosis inducing factor


Bcl-2 homology domain


high temperature requirement protein A2


optic atrophy type 1 protein


second mitochondria derived activator of caspase/direct IAP binding protein with low pI


tumor necrosis factor


TNF related apoptosis inducing ligand


X-linked inhibitor of apoptosis

Copyright information

© MAIK “Nauka/Interperiodica” 2005

Authors and Affiliations

  1. 1.Apoptose et Systeme ImmunitaireInstitut Pasteur, CNRS-URA 1961ParisFrance

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