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].