Oxidative stress as a regulator of murine atherosclerosis.
Altered cellular production of reactive oxygen species (ROS) and/or reactive nitrogen species (RNS) is a ubiquitous feature of human disease. Vascular oxidative stress is a unifying area of research in atherosclerosis and aging. While elevated levels of ROS, especially oxygen radicals (O2-) and hydrogen peroxide (H2O2), induce cellular apoptosis, low levels play an important role in cell signaling [1,2]. Reactive species from a variety of sources further play an important role in plaque disruption partly through lipid oxidation, low-density lipoprotein oxidation nitration, and signaling [3-6].
Hsiai
Tzung
T
Biomedical Engineering & Cardiovascular Medicine, University of Southern California, Los Angeles, CA 90089, USA.
Berliner
Judith A
JA
D000375:Aging; D000818:Animals; D017209:Apoptosis / Q000502:physiology; D050197:Atherosclerosis / Q000473:pathology*; D004195:Disease Models, Animal; D051379:Mice; D018384:Oxidative Stress / Q000502:physiology*; D026361:Reactive Nitrogen Species / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015398:Signal Transduction
D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species