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Oxidative Stress and Vascular Disease pp 135–154Cite as

Oxidation-Sensitive Transcription and Gene Expression in Atherosclerosis

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Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 224))

Abstract

Historically, most research into the role of oxidative stress and reactive oxygen species (ROS) in inflammatory diseases such as rheumatoid arthritis, pulmonary emphysema, neurodegenerative disorders and atherosclerosis has focused on the putative role of ROS as cellular damaging agents through the potential toxic oxidative modification of macromolecules such as proteins, lipids and DNA and on the cytotoxicity of free radicals and their reaction products (1). In this context, ROS have been viewed as playing a destructive role in biology. Although this may be true for high concentrations of ROS, many cell types such as fibroblasts, endothelial cells and smooth muscle cells have been shown to produce ROS at relatively low levels where they play a role as intracellular messenger molecules. In this context, ROS serve as physiological second messengers to regulate signal transduction pathways that ultimately control gene expression and post-translational modifications of proteins.

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Authors
  1. Charles Kunsch
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  2. Russell M. Medford
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Editors and Affiliations

  1. Boston University School of Medicine, Boston, MA, USA

    John F. Keaney Jr. M.D. (Associate Professor of Medicine and Pharmacology) (Associate Professor of Medicine and Pharmacology)

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Kunsch, C., Medford, R.M. (2000). Oxidation-Sensitive Transcription and Gene Expression in Atherosclerosis. In: Keaney, J.F. (eds) Oxidative Stress and Vascular Disease. Developments in Cardiovascular Medicine, vol 224. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-4649-8_8

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  • DOI: https://doi.org/10.1007/978-1-4615-4649-8_8

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