Biotechnology and Molecular Biology Reviews

  • Abbreviation: Biotechnol. Mol. Biol. Rev.
  • Language: English
  • ISSN: 1538-2273
  • DOI: 10.5897/BMBR
  • Start Year: 2006
  • Published Articles: 102


Homocysteine and cardiovascular disease

Dwivedi M. K.1,2*, Tripathi A. K.2, Shukla S.2,  Khan S.1 and Chauhan U. K.2
1Department of Post-graduate Studies and Research in Biological Sciences, Rani Durgawati University Jabalpur, Madhya Pradesh (M. P.) India. 2Study Centre for Biotechnology, Awadhesh Pratap Singh University, Madhya Pradesh (Rewa M. P.) India.
Email: [email protected]

  •  Accepted: 24 January 2011
  •  Published: 31 January 2011


Based on prospective and experimental data, mild to moderate elevation of homocysteine is a stabilized and independent risk factor for cardiovascular disease. The hyperhomocystenemia is a consequence of inhibition of transsulphuration pathway or inhibition of remethylation pathway of homocysteine metabolism, transsulphuration is mediated by CBS and remethylation is mediated directly by MS and indirectly by MTHFR. The SNPs in these genes alter the activity of corresponding proteins hence it may or may not be responsible for mild to moderate hyperhomocysteinemia. The consequences of hyperhomocysteinemia arise in the form of endothelial cell injury by increased oxidative stress and reduced bioavailability of nitric oxide, increased platelet adhesiveness, enhanced LDL deposition on arterial wall and activation of coagulation cascade. Some environmental factors are also known to contribute in progression toward disease.


Key words: Homocysteine, oxidative stress, inflammation.


Hyc, Homocysteine; CAD, cardio vascular disease; MTHFR, methylene tetrahydro folate reductase; CBS
cystathionine beta syntheses; MS, methinine synthase; SAM, S- adinosyl methonine; SAH, S- adinosyl homocysteine; Tm, transition metal; SOD, super oxide dismutase; RS-H, free thiol; NO, nitric oxide; LDL, low density lipid; OxLDL, oxidised low density lipid; CP, ceruloplasmin; Cb, cynocobalamine