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World J Cardiol. Jun 26, 2014; 6(6): 462-477
Published online Jun 26, 2014. doi: 10.4330/wjc.v6.i6.462
Published online Jun 26, 2014. doi: 10.4330/wjc.v6.i6.462
Antioxidants, inflammation and cardiovascular disease
Harald Mangge, Research Unit on Lifestyle and Inflammation associated Risk Biomarkers, Clinical Institute of Medical and Chemical Laboratory Diagnosis, Medical University of Graz, 8036 Graz, and BioTechMed-Graz, Austria
Kathrin Becker, Dietmar Fuchs, Division of Biological Chemistry, Biocenter, Innsbruck Medical University, 6020 Innsbruck, Austria
Johanna M Gostner, Division of Medical Biochemistry, Biocenter, Innsbruck Medical University, 6020 Innsbruck, Austria
Author contributions: Each of the authors has made a substantial contribution so as to qualify for authorship; and all authors have read and approved the paper.
Correspondence to: Dr. Dietmar Fuchs, Division of Biological Chemistry, Biocenter, Innsbruck Medical University, Innrain 80, 6020 Innsbruck, Austria. dietmar.fuchs@i-med.ac.at
Telephone: +43-512-900370350 Fax: +43-512-900373110
Received: January 7, 2014
Revised: March 26, 2014
Accepted: April 17, 2014
Published online: June 26, 2014
Revised: March 26, 2014
Accepted: April 17, 2014
Published online: June 26, 2014
Core Tip
Core tip: Crosstalk between a number of pathways involved in the regulation of immune and endothelial homeostasis is strongly coordinated by redox processes. Underlying molecular mechanisms of atherogenesis include metabolic imbalances that are linked to the onset and progression of endothelial dysfunction and inflammation, finally leading to a status of heightened oxidative stress. Decrease of plasma antioxidants may develop secondarily due to an increased demand for oxidation-sensitive vitamins during inflammation. Antioxidant and vitamin supplementation therapy is controversially discussed and success might depend of an individual patient’s demand.