Abstract

REVIEW A variety of key events in apoptosis focus on mitochondria, including the release of caspase activators (such as cytochrome c), changes in electron transport, loss of mitochondrial transmembrane potential, altered cellular oxidation-reduction, and participation of pro- and antiapoptotic Bcl-2 family proteins. The different signals that converge on mitochondria to trigger or inhibit these events and their downstream effects delineate several major pathways in physiological cell death.

Keywords

MitochondrionApoptosisCell biologyCytochrome cBcl-2 familyElectron transport chainProgrammed cell deathCaspaseBiologyChemistryBiochemistry

MeSH Terms

AnimalsApoptosisCysteine EndopeptidasesCytochrome c GroupElectron TransportHumansIntracellular MembranesIon ChannelsMembrane PotentialsMitochondriaOxidation-ReductionPermeabilityProto-Oncogene Proteins c-bcl-2

Affiliated Institutions

Related Publications

Publication Info

Year
1998
Type
review
Volume
281
Issue
5381
Pages
1309-1312
Citations
8944
Access
Closed

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Citation Metrics

8944
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73
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7351
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Cite This

Douglas R. Green, John C. Reed (1998). Mitochondria and Apoptosis. Science , 281 (5381) , 1309-1312. https://doi.org/10.1126/science.281.5381.1309

Identifiers

DOI
10.1126/science.281.5381.1309
PMID
9721092

Data Quality

Data completeness: 81%