New insights into mitochondrial structure during cell death

    Authors

    G. Perkins; E. Bossy-Wetzel;M. H. Ellisman

    Comments

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    Abbreviated Journal Title

    Exp. Neurol.

    Keywords

    Apoptosis; Cardiolipin; Crista junction; Cristae remodeling; Cytochrome; c; Electron tomography; Mitochondria; Neurodegeneration; OPA1; CYTOCHROME-C RELEASE; AMYOTROPHIC-LATERAL-SCLEROSIS; PAINFUL PERIPHERAL; NEUROPATHY; SUPEROXIDE-DISMUTASE SOD1; SYNUCLEIN TRANSGENIC MICE; DYNAMIN-RELATED GTPASE; INNER-MEMBRANE; OXIDATIVE STRESS; ENDOPLASMIC-RETICULUM; ELECTRON TOMOGRAPHY; Neurosciences

    Abstract

    Mitochondria play a pivotal role in the cascade of events associated with cell death pathways that are involved with several forms of neurodegeneration. Recent findings show that in the Bax/Bak-dependent pathway of apoptosis, the release of cytochrome c from mitochondria is a consequence of two carefully coordinated events: opening of crista junctions triggered by OPA1 oligomer disassembly and formation of outer membrane pores. Both steps are necessary for the complete release of pro-apoptotic proteins. The remodeling of mitochrondrial structure accompanies this pathway, including mitochondrial fission, and cristae and crista junction alterations. Yet, there is controversy surrounding the timing of certain remodeling events and whether they are necessary early events required for the release of pro-apoptotic factors or are simply a downstream after-effect. Here, we analyze the current knowledge of mitochondrial remodeling during cell death and discuss what structural alterations Occur to this organelle during neurodegeneration, focusing Oil the higher resolution structural correlates obtained by electron microscopy and electron tomography. (C) 2009 Elsevier Inc. All rights reserved.

    Journal Title

    Experimental Neurology

    Volume

    218

    Issue/Number

    2

    Publication Date

    1-1-2009

    Document Type

    Review

    Language

    English

    First Page

    183

    Last Page

    192

    WOS Identifier

    WOS:000268117400003

    ISSN

    0014-4886

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