Mitochondria, oxidative metabolism and cell death in stroke
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...stroke-related research (for review, see Niizuma et al., 2009; Sims and Muyderman, 2010), as mitochondrial changes following glu-...
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...Mitochondria are and have been the focus of a vast amount of stroke-related research (for review, see Niizuma et al., 2009; Sims and Muyderman, 2010), as mitochondrial changes following glucose–oxygen deprivation, such as decreased ATP production and increased ROS production, contribute to…...
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References
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"Mitochondria, oxidative metabolism ..." refers background in this paper
...IAPs inhibit caspase-3, caspase-7 and caspase-9....
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...Endonuclease G, another protein released from mitochondria, can interact with AIF under some conditions and can directly cause caspase-independent apoptosis [3,25,26]....
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...Interactions of AIF with the protein, cyclophin A in the cytosol and co-translocation of the two proteins lead to DNA degradation [3,25,26,100]....
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...1), which result from mitochondrial release of apoptosis inducing factor (AIF) and perhaps other proteins [3,25,26], have also been implicated in focal ischemic damage (see section 5....
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...Omi/HtrA2 but not Smac/DIABLO has a proteolytic activity that contributes to the inhibitory effects on IAPs [3,25]....
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"Mitochondria, oxidative metabolism ..." refers background in this paper
...This “penumbral” or “perifocal” tissue typically exhibits reductions to approximately 20–40% of normal flow [8,9,12]....
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...Neurons in the penumbra are electrically silent for long periods, a response associated with hyperpolarization of the plasma membrane [8,12]....
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