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Anti-inflammatory strategies for homocysteine-related cardiovascular disease
Chih-Pei Lin1, Yung-Hsiang Chen, Hsin-Bang Leu
1Faculty of Biotechnology and Laboratory Science in Medicine, Institute of Biotechnology in Medicine, National Yang-Ming University, Taipei, Taiwan.
Insights
High homocysteine levels contribute to atherosclerosis and vascular damage. While vitamin supplementation is suggested, evidence for reducing cardiovascular disease risk is limited, highlighting the need for further research.
Area of Science:
- Cardiovascular Science
- Vascular Biology
- Biochemistry
Background:
- Homocysteine is implicated in vascular damage and atherosclerosis.
- Vitamin/folate supplementation is proposed to mitigate cardiovascular disease risk.
- Current randomized trials lack definitive proof of homocysteine reduction's efficacy in lowering cardiovascular disease incidence.
Purpose of the Study:
- To review evidence on the homocysteine-cardiovascular disease association.
- To discuss the relevance of screening, treatment, and prevention for hyperhomocysteinemia-related cardiovascular disease.
- To explore potential therapeutic strategies targeting inflammation and oxidative stress.
Main Methods:
- Literature review of existing evidence.
- Analysis of homocysteine's role in oxidative stress and endothelial dysfunction.
- Examination of previous findings on mononuclear cell activation and statin effects.
Main Results:
- Homocysteine induces oxidative stress, endothelial dysfunction, lipid peroxidation, and inflammation, accelerating atherosclerosis.
- Mononuclear cell activation plays a significant role in homocysteine-induced endothelial dysfunction.
- Statins demonstrated novel endothelial protection by attenuating homocysteine-induced endothelial adhesiveness.
Conclusions:
- Inflammation and oxidative stress are key mediators of homocysteine-induced vascular damage.
- Targeting endothelial dysfunction and mononuclear cell activation with anti-inflammatory/antioxidative agents offers potential therapeutic strategies.
- Further research is needed to clarify the clinical utility of homocysteine screening and intervention for cardiovascular disease prevention.
Abstract:
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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