In 1969, McCully first proposed that homocysteine, an amino acid produced during catabolism of methionine, causes arterial and venous atherothrombotic disease.1 This theory was based on observations that children with extreme elevations of plasma homocysteine concentrations due to inborn errors of metabolism also had premature atherothrombotic disease. While the genetic disorders associated with homocystinuria are rare, these conditions provide an in vivo human model for vascular injury associated with exposure to high homocysteine concentrations. Subsequent in vitro and in vivo studies confirmed that in experimental settings, homocysteine can cause atherothrombosis by promoting oxidative stress, endothelial cell damage, endothelial dysfunction, inflammation, thrombosis, and cell proliferation.2
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