Mutation Study Of Homocysteine Metabolism-related Enzyme Genes And Treatment Of Hyperhomocysteinemia In Patients With Coronary Heart Disease

Mutation Study of Homocysteine Metabolism-related Enzyme Genes and Treatment of Hyperhomocystememia in Patients withCoronary Heart DiseaseThe conventional risk factors for coronary heart disease (CHD) include smoking, hypertension, hyperlipidemia and diabetes mellitus. In recent years, hyperhomocysteinemia has received greater attention as a possible important risk factor for atherosclerosis and coronary artery disease. Homocysteine (Hcy) may cause endothelial cell injury, promote proliferation and migration of vascular smooth muscle cells, increase adhesiveness and aggregation of platelets, activate many factors involved in the clotting cascade and reduce antithrombin activity. It may lead to increase susceptibility of low density lipoprotein to oxidation that makes them more atherogenic.Hcy is an intermediate during the metabolism of methionine. Then Hcy enters either the transsulfuration pathway or the remethylation cycle. In the former pathway, the vitamin B₆-dependent Cystathionine P-synthase (CBS) binds homocysteine to serine to form cystathionine. In the latter pathway, Hcy requires vitamin B₁₂-dependent Methionine Synthase (MS) to form methionine . Methylcobalamin and methyltetrahydrofolate serve as cofactor and cosubstrate for this enzyme. Methylenetetrahydrofolate Reductase (MTHFR) is also an essential enzyme in this cycle. The causes of hyperhomocysteinemia are multifactorial. Genetic factors include low activities of MTHFR, CBS and MS due to gene...