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2008•European Cardiology ReviewOpen access

Homocysteine-lowering Treatment in Reduction of Stroke and Coronary Vascular Risk – Do Not Give Up

Wolfgang R. Herrmann, Rima Obeid

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Abstract

Homocysteine (Hcy) is a non-essential, non-protein-forming amino acid that originates in methionine via a transmethylation reaction. Hcy is catabolized into methionine or cysteine. Methionine synthase and its co-factor, methylcobalamin, enhance the methylation of Hcy into methionine, where 5-methyl tetrahydrofolate donates its methyl group to Hcy. The trans-sulfuration pathway of Hcy catabolism is mediated via cystathionine beta synthase (CBS) and cystathionase, both of which are vitamin-B6-dependent.

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Homocysteine (Hcy) is a non-essential, non-protein-forming amino acid that originates in methionine via a transmethylation reaction. Hcy is catabolized into methionine or cysteine. Methionine synthase and its co-factor, methylcobalamin, enhance the methylation of Hcy into methionine, where 5-methyl tetrahydrofolate donates its methyl group to Hcy. The trans-sulfuration pathway of Hcy catabolism is mediated via cystathionine beta synthase (CBS) and cystathionase, both of which are vitamin-B6-dependent.

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Available abstract

Homocysteine (Hcy) is a non-essential, non-protein-forming amino acid that originates in methionine via a transmethylation reaction. Hcy is catabolized into methionine or cysteine. Methionine synthase and its co-factor, methylcobalamin, enhance the methylation of Hcy into methionine, where 5-methyl tetrahydrofolate donates its methyl group to Hcy. The trans-sulfuration pathway of Hcy catabolism is mediated via cystathionine beta synthase (CBS) and cystathionase, both of which are vitamin-B6-dependent.

Key concepts: Transmethylation, Homocysteine, Cystathionine beta synthase, Methylcobalamin, Methionine synthase, Methionine, Cysteine, Biochemistry

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