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[Homocysteine--a risk factor for atherosclerosis]
1Siklósi Kórház Kht., Belgyógyászati Osztály.
Insights
Elevated homocysteine is a risk factor for vascular disease, potentially caused by genetic factors or vitamin deficiencies. Folic acid, vitamin B12, and B6 are crucial for maintaining normal homocysteine levels and endothelial health.
Area of Science:
- Cardiovascular Medicine
- Biochemistry
- Nutritional Science
Context:
- Elevated plasma homocysteine is recognized as a significant risk factor for atherosclerotic vascular disease.
- This condition, known as hyperhomocysteinemia, contributes to atherogenesis in peripheral, coronary, and cerebrovascular arteries.
- It can arise from genetic mutations affecting key enzymes or deficiencies in essential B vitamins.
Purpose:
- To elucidate the mechanisms by which elevated homocysteine contributes to vascular disease.
- To explore the role of oxidative stress and endothelial dysfunction in homocysteine-induced injury.
- To highlight the importance of B vitamins in managing homocysteine levels and vascular health.
Summary:
- Hyperhomocysteinemia, caused by genetic or nutritional factors, promotes atherosclerosis.
- Homocysteine induces endothelial damage via oxidative stress and impairs anticoagulant pathways.
- Reduced levels of protective enzymes like glutathione peroxidase exacerbate oxidative injury.
- Folic acid, vitamin B12, and vitamin B6 are vital for regulating homocysteine and preserving endothelial function.
Impact:
- Understanding these mechanisms can inform strategies for preventing and managing vascular diseases.
- Targeting homocysteine levels through nutritional interventions may mitigate cardiovascular and cerebrovascular risks.
- This research underscores the critical role of B vitamins in maintaining vascular integrity and preventing disease progression.
Abstract:
Elevated plasma homocysteine is a new risk factor for atherosclerotic vascular disease resulting in progressive atherogenesis in the arteries of the limbs, the coronary arteries and the cerebrovascular system. Hyperhomocysteinemia may be induced by failure or decreased enzyme activity of the cystathionine-beta-synthase and methylenetetrahydrofolate reductase due to genetic mutation or deficiency of folic acid, vitamin B12 and vitamin B6. Oxidation of homocysteine to homocystine is accompanied with production of hydrogen peroxide inducing damage of endothelium through oxidative stress. The injury of the endothelium by homocysteine can be shown by measuring flow-induced vasodilation in men. The abnormalities of coagulation found in hyperhomocysteinemia is related to the impairment of the function of endothelial cells and inhibition of the thrombomodulin-protein C and glycosaminoglycan-antithrombin-III anticoagulant system. Homocysteine decreases the level of glutathione peroxidase in the endothelial cells, and inhibits its activation leading to the impairment of oxidative defensive mechanism, and to the free radical-induced NO-inactivation. In decreasing of plasma homocysteine level and preventing its influence on endothelium, moreover in improving of endothelial function the folic acid has cardinal importance, however the vitamin B12 and vitamin B6 also play role in the maintenance of normal homocysteine level of blood.