Atherosclerosis as disease of redox-sensitive genes.
Year: 1998
Type: review
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.
Source: PubMed
Author: R W Alexander
Institution: Emory University
Language: English
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W197537679