IMR Press / FBL / Volume 14 / Issue 10 / DOI: 10.2741/3492

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article
Anti-inflammatory strategies for homocysteine-related cardiovascular disease
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1 Faculty of Biotechnology and Laboratory Science in Medicine, Institute of Biotechnology in Medicine, National Yang-Ming University, Taipei, Taiwan
2 Institute of Public Health, National Yang-Ming University, Taipei, Taiwan
3 Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan
4 Institute of Pharmacology, National Yang-Ming University, Taipei, Taiwan
5 Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan
6 Graduate Institute of Integrated Medicine, College of Chinese Medicine, China Medical University, Taichung, Taiwan
7 Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan
8 Division of Cardiology, Taipei Veterans General Hospital, Taipei, Taiwan
9 Department of Anatomy and Cell Biology, College of Medicine, National Taiwan University, Taipei, Taiwan

Academic Editor: Jaw-Wen Chen

Front. Biosci. (Landmark Ed) 2009, 14(10), 3836–3845;
Published: 1 January 2009

Homocysteine may induce vascular damage for atherosclerosis. Vitamin/folate supplementation has been proposed to reduce the cardiovascular disease risk. Nevertheless, there is no randomized clinical trial clearly proving the efficacy of reducing the homocysteine as a means of lowering the incidence of cardiovascular disease. Homocysteine induces oxidative stress leading to endothelial dysfunction. In addition, homocysteine-induced oxidative stress favors lipid peroxidation and induces production of inflammatory factors, thus accelerating atherosclerosis. In this paper, we reviewed the available evidence concerning the association between homocysteine and cardiovascular disease, with the objective of discussing the pertinence of screening, treatment, and prevention of hyperhomocysteinemia-related cardiovascular disease. Our previous findings also indicated the significant role of mononuclear cells activation in homocysteine-induced endothelial dysfunction; treatment with statins attenuated homocysteine-induced endothelial adhesiveness, indicating the novel endothelial protection effects of statins in the presence of homocysteine. Since inflammation and oxidative stress are critical to homocysteine-induced vascular damage, the improvement of endothelial dysfunction and the inhibition of mononuclear cell activation by anti-inflammatory and/or antioxidative drugs/agents may serve as the potential therapeutic strategy for hyperhomocysteinemia-related cardiovascular disease.

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