Journal
CURRENT MEDICINAL CHEMISTRY
Volume 15, Issue 21, Pages 2157-2172Publisher
BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/092986708785747634
Keywords
Atherosclerosis; apoptosis; iron chemistry; signaling pathways; immunity; transcription factors; iron binding/regulatory proteins
Funding
- Swedish Research Council
- Swedish Heart Lung Foundation
- Cardiovascular Inflammation Research Center of Linkoping University
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Atherosclerosis being a leading death cause in many countries is a chronic inflammatory process in which inflammation, immune activation, and oxidative stress are interactively involved. Some epidemiological and many experimental studies suggest that development of atherosclerosis is associated with the amount of iron stored in the body. Transport of electrons between different forms of iron makes it essential for many fundamental cell functions and signaling. Under pathologic conditions iron may serves as a potential catalyst, particularly in the form of redox-active iron or labile iron, for free radical reactions in oxidative stress and cell damage of atherogenesis. Emerging evidence indicates that cellular iron may participate in various cellular signaling pathways, many of which have been implicated in atherogenesis. These include iron homeostatic control signaling, iron-induced oxidative-responsive transcription factors, iron-induced activation of inflammatory cytokines, and iron-dependent signaling in cell growth and apoptosis. This review highlights research progress on atherosclerosis-relevant iron signaling and revisits our hypothesis on iron and atherosclerosis. We propose that iron may contribute to the pathogenesis of atherosclerosis not only via changes in the body iron amount but also by its regulatory roles in redox-sensitive signaling and inflammatory immune responses of atherosclerosis
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