Redox signals that regulate the vascular response to injury.
Multiple enzymes may stimulate ROS production in VSMC and endothelial cells. These include NADH/NADPH oxidase, xanthine oxidase, lipoxygenases, cyclooxygenase, P-450 monooxygenases, and the enzymes of mitochondrial oxidative phosphorylation. In addition to generation of intracellular O2- by these enzymes, extracellular stimuli including lipophilic substrates, membrane permeant oxidants (e.g., H2O2), cytokines, and growth factors may modulate cellular redox state. Both intracellular and extracellular ROS act as second-messengers to activate tyrosine and serine-threonine kinases, such as the MAP kinase family. As discussed in the previous sections, regulation of the MAP kinases is one example of the complexity of ROS-dependent signal transduction. Although the complexity of ROS-mediated signal transduction is daunting, the diversity offers multiple therapeutic targets for pharmacologic intervention.
Berk
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BC
Center for Cardiovascular Research, University of Rochester, NY 14642, USA. bradford_berk@urmc.rochester.edu
D000818:Animals; D001808:Blood Vessels / Q000293:injuries* / Q000502:physiology; D005786:Gene Expression Regulation; D006801:Humans; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D011505:Protein-Tyrosine Kinases; D017382:Reactive Oxygen Species; D015398:Signal Transduction
D017382:Reactive Oxygen Species; D011505:Protein-Tyrosine Kinases