The mitochondrial death/life regulator in apoptosis and necrosis.

@article{Kroemer1998TheMD,
  title={The mitochondrial death/life regulator in apoptosis and necrosis.},
  author={Guido Kroemer and Bruno Dallaporta and Mich{\`e}le Resche-Rigon},
  journal={Annual review of physiology},
  year={1998},
  volume={60},
  pages={619-42}
}
Both physiological cell death (apoptosis) and, in some cases, accidental cell death (necrosis) involve a two-step process. At a first level, numerous physiological and some pathological stimuli trigger an increase in mitochondrial membrane permeability. The mitochondria release apoptogenic factors through the outer membrane and dissipate the electrochemical gradient of the inner membrane. Mitochondrial permeability transition (PT) involves a dynamic multiprotein complex formed in the contact… CONTINUE READING
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Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
At a second level , the consequences of mitochondrial dysfunction ( collapse of the mitochondrial inner transmembrane potential , uncoupling of the respiratory chain , hyperproduction of superoxide anions , disruption of mitochondrial biogenesis , outflow of matrix calcium and glutathione , and release of soluble intermembrane proteins ) entails a bioenergetic catastrophe culminating in the disruption of plasma membrane integrity ( necrosis ) and/or the activation of specific apoptogenic proteases ( caspases ) by mitochondrial proteins that leak into the cytosol ( cytochrome c , apoptosis - inducing factor ) with secondary endonuclease activation ( apoptosis ) .
At a second level , the consequences of mitochondrial dysfunction ( collapse of the mitochondrial inner transmembrane potential , uncoupling of the respiratory chain , hyperproduction of superoxide anions , disruption of mitochondrial biogenesis , outflow of matrix calcium and glutathione , and release of soluble intermembrane proteins ) entails a bioenergetic catastrophe culminating in the disruption of plasma membrane integrity ( necrosis ) and/or the activation of specific apoptogenic proteases ( caspases ) by mitochondrial proteins that leak into the cytosol ( cytochrome c , apoptosis - inducing factor ) with secondary endonuclease activation ( apoptosis ) .
At a second level , the consequences of mitochondrial dysfunction ( collapse of the mitochondrial inner transmembrane potential , uncoupling of the respiratory chain , hyperproduction of superoxide anions , disruption of mitochondrial biogenesis , outflow of matrix calcium and glutathione , and release of soluble intermembrane proteins ) entails a bioenergetic catastrophe culminating in the disruption of plasma membrane integrity ( necrosis ) and/or the activation of specific apoptogenic proteases ( caspases ) by mitochondrial proteins that leak into the cytosol ( cytochrome c , apoptosis - inducing factor ) with secondary endonuclease activation ( apoptosis ) .
Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
Inhibition of PT by pharmacological intervention on mitochondrial structures or mitochondrial expression of the apoptosis - inhibitory oncoprotein Bcl-2 prevents cell death , suggesting that PT is a rate - limiting event of the death process .
Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
The mitochondrial death / life regulator in apoptosis and necrosis .
Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
The mitochondrial death / life regulator in apoptosis and necrosis .
At a second level , the consequences of mitochondrial dysfunction ( collapse of the mitochondrial inner transmembrane potential , uncoupling of the respiratory chain , hyperproduction of superoxide anions , disruption of mitochondrial biogenesis , outflow of matrix calcium and glutathione , and release of soluble intermembrane proteins ) entails a bioenergetic catastrophe culminating in the disruption of plasma membrane integrity ( necrosis ) and/or the activation of specific apoptogenic proteases ( caspases ) by mitochondrial proteins that leak into the cytosol ( cytochrome c , apoptosis - inducing factor ) with secondary endonuclease activation ( apoptosis ) .
Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
Both physiological cell death ( apoptosis ) and , in some cases , accidental cell death ( necrosis ) involve a two - step process .
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