Therapeutical approach on plasma homocysteine and cardiovascular risk reduction

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Abstract

Homocysteine is a sulfur-containing aminoacid produced during metabolism of methionine. Since 1969 the relationship between altered homocysteine metabolism and both coronary and peripheral atherotrombosis is known; in recent years experimental evidences have shown that elevated plasma levels of homocysteine are associated with an increased risk of atherosclerosis and cardiovascular ischemic events. Several mechanisms by which elevated homocysteine impairs vascular function have been proposed, including impairment of endothelial function, production of reactive oxygen species (ROS) and consequent oxidation of low-density lipids. Endothelial function is altered in subjects with hyperhomocysteinemia, and endothelial dysfunction is correlated with plasma levels of homocysteine. Folic acid and B vitamins, required for remethylation of homocysteine to methionine, are the most important dietary determinants of homocysteine and daily supplementation typically lowers plasma homocysteine levels; it is still unclear whether the decreased plasma levels of homocysteine through diet or drugs may be paralleled by a reduction in cardiovascular risk.
Lingua originaleEnglish
pagine (da-a)219-224
Numero di pagine6
RivistaTherapeutics and Clinical Risk Management
Volume4
Stato di pubblicazionePublished - 2008

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All Science Journal Classification (ASJC) codes

  • Safety Research
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Pharmacology (medical)
  • Chemical Health and Safety

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