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Abstract

Homocysteine, an amino acid in the blood, is increasingly recognized as a significant risk factor for atherosclerosis. Elevated levels of homocysteine contribute to oxidative stress and endothelial damage, leading to platelet aggregation and plaque formation within blood vessel walls. This process results in the narrowing of blood vessels and the progression of atherosclerosis. Elevated homocysteine levels reduce nitric oxide availability, heighten intracellular oxidative stress, and activate various pro-atherogenic pathways. Current therapeutic strategies focus on reducing homocysteine levels through supplementation with vitamin B6, B12, folic acid, betaine, and 5-methyl tetrahydrofolate. Ongoing clinical trials are exploring the efficacy of folate-based therapies in managing homocysteine levels and mitigating associated cardiovascular risks.