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Clinical Chemistry and Laboratory Medicine (CCLM)

Published in Association with the European Federation of Clinical Chemistry and Laboratory Medicine (EFLM)

Editor-in-Chief: Plebani, Mario

Ed. by Gillery, Philippe / Lackner, Karl J. / Lippi, Giuseppe / Melichar, Bohuslav / Payne, Deborah A. / Schlattmann, Peter / Tate, Jillian R.

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1437-4331
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Volume 45, Issue 12 (Dec 2007)

Issues

The molecular basis of homocysteine thiolactone-mediated vascular disease

Hieronim Jakubowski
  • 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
Published Online: 2007-12-08 | DOI: https://doi.org/10.1515/CCLM.2007.338

Abstract

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

About the article

Corresponding author: Hieronim Jakubowski, PhD, Department of Microbiology and Molecular Genetics, UMDNJ-New Jersey Medical School, International Center for Public Health, 225 Warren Street, Newark, NJ 07101-1709, USA Phone: +1-973-972-4483, Fax: +1-973-972-8982,


Received: 2007-06-20

Accepted: 2007-08-29

Published Online: 2007-12-08

Published in Print: 2007-12-01


Citation Information: Clinical Chemical Laboratory Medicine, ISSN (Online) 14374331, ISSN (Print) 14346621, DOI: https://doi.org/10.1515/CCLM.2007.338. Export Citation

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