Clinical Chemistry and Laboratory Medicine (CCLM)
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The molecular basis of homocysteine thiolactone-mediated vascular disease
- 1Department of Microbiology and Molecular Genetics, UMDNJ-New Jersey Medical School, International Center for Public Health, Newark, USA and Institute of Bioorganic Chemistry, Polish Academy of Sciences, Poznań, Poland
Accumulating evidence suggests that a metabolite of homocysteine (Hcy), the thioester Hcy-thiolactone, plays an important role in atherogenesis and thrombosis. Hcy-thiolactone levels are elevated in hyperhomocysteinemic humans and mice. The thioester chemistry of Hcy-thiolactone underlies its ability to form isopeptide bonds with protein lysine residues, which impairs or alters the protein's function. Protein targets for the modification by Hcy-thiolactone in human blood include fibrinogen, low-density lipoprotein, and high-density lipoprotein. Protein N-homocysteinylation leads to pathophysiological responses, including increased susceptibility to thrombogenesis caused by N-Hcy-fibrinogen, and an autoimmune response elicited by N-Hcy-proteins. Chronic activation of these responses in hyperhomocysteinemia over many years could lead to vascular disease. This article reviews recent evidence supporting the hypothesis that Hcy-thiolactone contributes to pathophysiological effects of Hcy on the vascular system.
Clin Chem Lab Med 2007;45:1704–16.
Keywords: atherosclerosis; autoantibodies; cystathionine β-synthase (CBS); dietary hyperhomocysteinemia; fibrinogen; genetic hyperhomocysteinemia; homocysteine thiolactone hypothesis; immune activation; methylenetetrahydrofolate reductase (MTHFR); protein N-homocysteinylation; thrombosis
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