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HOMOCYSTEINE AND CARDIOVASCULAR DISEASE - A CURRENT REVIEW
Alicja Gospodarczyk1, Kamil Marczewski2, Natalia Gospodarczyk2
1DEPARTMENT OF BIOCHEMISTRY, MEDICAL UNIVERSITY OF SILESIA, KATOWICE, POLAND.
Insights
High homocysteine levels (hyperhomocysteinemia) contribute to atherosclerosis and cardiovascular diseases. Genetic mutations like MTHFR exacerbate this risk, increasing the likelihood of heart attack and stroke.
Area of Science:
- Cardiovascular Science
- Biochemistry
- Genetics
Background:
- Cardiovascular diseases, particularly ischemic heart disease, are the leading global cause of death.
- Atherosclerosis of the coronary arteries underlies over 98% of ischemic heart disease cases.
- Hyperhomocysteinemia, elevated homocysteine levels, is a significant risk factor for vascular damage and thrombotic complications.
Approach:
- This paper reviews evidence linking homocysteine metabolism and cardiovascular pathology.
- Mechanisms of homocysteine's adverse vascular effects are examined, including receptor activation and oxidative stress.
- The role of methylenetetrahydrofolate reductase (MTHFR) gene mutations in hyperhomocysteinemia and disease susceptibility is discussed.
Key Points:
- Homocysteine, an amino acid metabolite, can promote atherosclerosis and thrombosis when its plasma concentration is elevated.
- Adverse vascular effects involve Toll-like 4 receptor activation, N-methyl-d-aspartate receptor activation, increased reactive oxygen species (ROS), and impaired nitric oxide synthesis.
- Elevated ROS correlates with increased pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) and adhesion molecules.
- MTHFR gene mutations impair homocysteine regulation, increasing predisposition to atherosclerosis, myocardial infarction, stroke, and coronary artery disease.
Conclusions:
- Hyperhomocysteinemia is a critical factor in the pathogenesis of numerous cardiovascular diseases.
- Understanding homocysteine's role provides targets for preventing and managing atherosclerosis and its complications.
Abstract:
Cardiovascular diseases remain the leading cause of death worldwide for the past 20 years. Of these, ischemic heart disease has the highest mortality rate. In over 98% of cases it is caused by atherosclerosis of the coronary arteries. Homocysteine is an amino acid, containing a sulfhydryl group, which is formed as a result of the metabolism of the amino acids methionine and cysteine, which is supplied with protein-containing foods. A small amount of it is necessary for the proper functioning of the body, however, an increased concentration in blood plasma, which hyperhomocysteinemia, negatively affects blood vessels leading to the development of atherosclerosis and thrombotic com¬plications. The adverse effect on blood vessels results from various mechanisms, such as: excessive activation of Toll-like 4 receptor, activation N-methyl-d-aspartate receptors, increased production of reactive oxygen species, and impairment of nitric oxide synthesis. Elevated levels of reactive oxygen species are associated with increased expression of proinflammatory cytokines such as IL-1β, IL-6, TNF-α (tumor necrosis tumor necrosis factor), MCP-1 and intracellular adhesion molecule-1. Another factor contributing to hyperhomocysteinemia is mutation of the MTHFR gene, which in normal conditions is responsible for maintaining homocysteine levels within the normal range. People with MTHFR mutation are more prone to develop atherosclerosis and the following complications: myocardial infarction, stroke, thrombotic episodes and coronary artery disease. The aim of this paper is to present evidence supporting the role of homocysteine in the development of many cardiovascular diseases.
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