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Transactions of the American Clinical and Climatological Association logoLink to Transactions of the American Clinical and Climatological Association
. 1998;109:129–146.

Atherosclerosis as disease of redox-sensitive genes.

R W Alexander 1
PMCID: PMC2194335  PMID: 9601133

Abstract

Accumulating evidence provides a compelling case that one of the major pathophysiologic mechanisms involved in the pathogenesis of atherosclerosis is enhanced oxidative stress and that the most important manifestation of this altered redox state is the modulation of a set(s) of proinflammatory genes that are regulated directly or indirectly by reactive oxygen species. Viewed in this perspective the oxidation of LDL is but one important consequence of a generalized metabolic abnormality of the arterial wall in atherosclerosis rather than being the core pathophysiological feature. The fact that hypercholesterolemia, hypertension, and AGEs related to diabetes mellitus all activate similar redox-sensitive proinflammatory genes associated with the pathogenesis of atherosclerosis provides the potential for the development of unifying concepts concerning the etiology of the disease. These concepts also provide additional evidence that antioxidants may be potentially attractive therapeutic agents.

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Selected References

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