Abstract
Reactive oxygen species (ROS) and mitochondria play an important role in apoptosis induction under both physiologic and pathologic conditions. Interestingly, mitochondria are both source and target of ROS. Cytochrome c release from mitochondria, that triggers caspase activation, appears to be largely mediated by direct or indirect ROS action. On the other hand, ROS have also anti-apoptotic effects. This review focuses on the role of ROS in the regulation of apoptosis, especially in inflammatory cells.
Original language | English |
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Pages (from-to) | 415-418 |
Number of pages | 4 |
Journal | Apoptosis |
Volume | 5 |
Issue number | 5 |
DOIs | |
State | Published - 2000 |
Bibliographical note
Funding Information:Work of the laboratory of H.U.S. is supported by the Swiss National Science Foundation (31-58916.99), the EMDO Foundation Zurich. Foundation Novartis Basel Helmut Horten Foundation Madonna del Piano, and Stiftung Zur Krebsbekämpting Zürich.
Keywords
- Apoptosis
- Death receptors
- Inflammation
- Reactive oxygen species (ROS)