Literature DB >> 15038600

Mitochondrial function in apoptotic neuronal cell death.

Samantha L Budd Haeberlein1.   

Abstract

Apoptosis can be defined as the regulated death of a cell and is conducted by conserved pathways. Apoptosis of neurons after injury or disease differs from programed cell death, in the sense that neurons in an adult brain are not "meant" to die and results in a loss of function. Thus apoptosis is an honorable process by a neuron, a cell with limited potential to replace itself, choosing instead to commit suicide to save neighboring cells from release of cellular components that cause injury directly or trigger secondary injury resulting from inflammatory reactions. The excess of apoptosis of neuronal cells underlies the progressive loss of neuronal populations in neurodegenerative disorders and thus is harmful. Mitochondria are the primary source for energy in neurons but are also poised, through the "mitochondrial apoptosis pathway," to signal the demise of cells. This duplicity of mitochondria is discussed, with particular attention given to the specialized case of pathological neuronal cell death.

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Year:  2004        PMID: 15038600     DOI: 10.1023/b:nere.0000014823.74782.b7

Source DB:  PubMed          Journal:  Neurochem Res        ISSN: 0364-3190            Impact factor:   3.996


  115 in total

1.  Mitochondria, calcium regulation, and acute glutamate excitotoxicity in cultured cerebellar granule cells.

Authors:  S L Budd; D G Nicholls
Journal:  J Neurochem       Date:  1996-12       Impact factor: 5.372

2.  Induction of apoptotic program in cell-free extracts: requirement for dATP and cytochrome c.

Authors:  X Liu; C N Kim; J Yang; R Jemmerson; X Wang
Journal:  Cell       Date:  1996-07-12       Impact factor: 41.582

3.  Mitochondrial cytochrome c release in apoptosis occurs upstream of DEVD-specific caspase activation and independently of mitochondrial transmembrane depolarization.

Authors:  E Bossy-Wetzel; D D Newmeyer; D R Green
Journal:  EMBO J       Date:  1998-01-02       Impact factor: 11.598

4.  Prevention of apoptosis by Bcl-2: release of cytochrome c from mitochondria blocked.

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Journal:  Science       Date:  1997-02-21       Impact factor: 47.728

5.  Bid, Bax, and lipids cooperate to form supramolecular openings in the outer mitochondrial membrane.

Authors:  Tomomi Kuwana; Mason R Mackey; Guy Perkins; Mark H Ellisman; Martin Latterich; Roger Schneiter; Douglas R Green; Donald D Newmeyer
Journal:  Cell       Date:  2002-11-01       Impact factor: 41.582

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Journal:  Int Rev Cytol       Date:  1980

7.  Exogenous smac induces competence and permits caspase activation in sympathetic neurons.

Authors:  Mohanish Deshmukh; Chunying Du; Xiaodong Wang; Eugene M Johnson
Journal:  J Neurosci       Date:  2002-09-15       Impact factor: 6.167

8.  Mechanisms of p75-mediated death of hippocampal neurons. Role of caspases.

Authors:  Carol M Troy; Jonathan E Friedman; Wilma J Friedman
Journal:  J Biol Chem       Date:  2002-07-03       Impact factor: 5.157

9.  Apocytochrome c blocks caspase-9 activation and Bax-induced apoptosis.

Authors:  Angel G Martin; Howard O Fearnhead
Journal:  J Biol Chem       Date:  2002-10-18       Impact factor: 5.157

10.  Bcl-2 inhibits the mitochondrial release of an apoptogenic protease.

Authors:  S A Susin; N Zamzami; M Castedo; T Hirsch; P Marchetti; A Macho; E Daugas; M Geuskens; G Kroemer
Journal:  J Exp Med       Date:  1996-10-01       Impact factor: 14.307

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  19 in total

1.  The effect of mild and severe hypoxia on rat cortical synaptosomes.

Authors:  C Aldinucci; A Carretta; G P Pessina
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Review 2.  Multifunctional drugs for head injury.

Authors:  Robert Vink; Alan J Nimmo
Journal:  Neurotherapeutics       Date:  2009-01       Impact factor: 7.620

3.  Paeoniflorin, a natural neuroprotective agent, modulates multiple anti-apoptotic and pro-apoptotic pathways in differentiated PC12 cells.

Authors:  Di Wang; Hei Kiu Wong; Yi-Bin Feng; Zhang-Jin Zhang
Journal:  Cell Mol Neurobiol       Date:  2013-02-24       Impact factor: 5.046

Review 4.  Natural Compounds as a Therapeutic Intervention following Traumatic Brain Injury: The Role of Phytochemicals.

Authors:  Stephen W Scheff; Mubeen A Ansari
Journal:  J Neurotrauma       Date:  2016-12-21       Impact factor: 5.269

5.  Temporal distribution of Hig-1 (hypoxia-induced gene 1) mRNA and protein in rat spinal cord: changes during postnatal life.

Authors:  Gabriela Bedó; Patricia Lagos; Daniella Agrati
Journal:  J Mol Neurosci       Date:  2012-02-16       Impact factor: 3.444

6.  Different proteolipid protein mutants exhibit unique metabolic defects.

Authors:  Maik Hüttemann; Zhan Zhang; Chadwick Mullins; Denise Bessert; Icksoo Lee; Klaus-Armin Nave; Sunita Appikatla; Robert P Skoff
Journal:  ASN Neuro       Date:  2009-08-25       Impact factor: 4.146

Review 7.  Translocator protein (18 kDa) TSPO: an emerging therapeutic target in neurotrauma.

Authors:  Vassilios Papadopoulos; Laurent Lecanu
Journal:  Exp Neurol       Date:  2009-05-04       Impact factor: 5.330

8.  Apoptosis-related genes change their expression with age and hearing loss in the mouse cochlea.

Authors:  Sherif F Tadros; Mary D'Souza; Xiaoxia Zhu; Robert D Frisina
Journal:  Apoptosis       Date:  2008-11       Impact factor: 4.677

9.  Do Autophagy Enhancers/ROS Scavengers Alleviate Consequences of Mild Mitochondrial Dysfunction Induced in Neuronal-Derived Cells?

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Journal:  Int J Mol Sci       Date:  2021-05-27       Impact factor: 5.923

10.  Embelin-induced apoptosis of HepG2 human hepatocellular carcinoma cells and blockade of HepG2 cells in the G2/M phase via the mitochondrial pathway.

Authors:  Asaf Taghiyev; Deguang Sun; Zhen Ming Gao; Rui Liang; Liming Wang
Journal:  Exp Ther Med       Date:  2012-07-11       Impact factor: 2.447

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