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||American English|
|Number of pages||4|
|Journal||Apoptosis : an international journal on programmed cell death|
|State||Published - 2000|
Bibliographical noteFunding 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.
- Death receptors
- Reactive oxygen species (ROS)