Bench-to-bedside review: Mitochondrial injury, oxidative stress and apoptosis – there is nothing more practical than a good theory
Year: 2008
Type: article
Abstract: Apoptosis contributes to cell death in common intensive care unit disorders such as traumatic brain injury and sepsis. Recent evidence suggests that this form of cell death is both clinically relevant and a potential therapeutic target in critical illness. Mitochondrial reactive oxygen species (ROS) have become a target for drug discovery in recent years since their production is characteristic of early stages of apoptosis. Among many antioxidant agents, stable nitroxide radicals targeted to mitochondria have attracted attention due to their ability to combine electron and free radical scavenging action with recycling capacities. Specific mechanisms of enhanced ROS generation in mitochondria and their translation into apoptotic signals are not well understood. This review focuses on several contemporary aspects of oxidative stress-mediated mitochondrial injury, particularly as they relate to oxidation of lipids and their specific signaling roles in apoptosis and phagocytosis of apoptotic cells.
Source: Critical Care
DOI: 10.1186/cc6779
Authors: Hülya Bayir, Valerian E Kagan
Institution: University of Pittsburgh
Language: English
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $4,190
Funders: American Heart Association, Laerdal Foundation for Acute Medicine, National Institutes of Health, U.S. Public Health Service, Eunice Kennedy Shriver National Institute of Child Health and Human Development, Medical Research and Materiel Command, Telemedicine and Advanced Technology Research Center
OpenAlex ID: W2136499248
