Homocysteine to methionine pathway

The homocysteine to methionine pathway (also called the homocysteine-methionine cycle or methionine remethylation pathway) is a fundamental metabolic process in human cells that remethylates homocysteine to methionine. Central enzymes include methionine synthase, which depends on vitamin B12 (cobalamin) as a cofactor and uses 5-methyltetrahydrofolate (from the folate cycle) as a methyl donor[2][6][4]. Methionine, as the end product, is necessary for protein synthesis and serves as the precursor for S-adenosylmethionine (SAM), the cell’s main methyl-group donor required for DNA, RNA, histone, and protein methylation reactions[1][2]. Dysfunction of this pathway, frequently due to deficiencies in vitamin B12, folate, or methylenetetrahydrofolate reductase (MTHFR), leads to increased homocysteine levels—an independent risk factor for cardiovascular, neurodegenerative, renal, and metabolic diseases[1][2][6]. This pathway is not itself a drug target, but its enzymes (methionine synthase, MTHFR, etc.) are molecular targets for nutritional or pharmacological intervention in hyperhomocysteinemia and associated disorders. Note: “Homocysteine to methionine pathway” is a metabolic pathway, not a specific molecular target (receptor, enzyme, etc.), so is_incorrect is true for structured drug target mapping[1][2][6].

Other names

Homocysteine-methionine cycleMethionine cycleRemethylation pathway

Enhancement of homocysteine remethylation via cofactors (e.g., folic acid, vitamin B12). Increase in methyl group availability (e.g., betaine as methyl donor).