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The molecular basis of homocysteine thiolactone-mediated vascular disease

Hieronim Jakubowski1

  • 1Department of Microbiology and Molecular Genetics, UMDNJ-New Jersey Medical School, International Center for Public Health, Newark, NJ 07101-1709, USA. jakubows@umdnj.edu

Clinical Chemistry and Laboratory Medicine
|October 17, 2007
PubMed

Insights

Homocysteine

Area of Science:

  • Biochemistry
  • Vascular Biology
  • Metabolomics

Background:

  • Elevated homocysteine (Hcy) levels are linked to vascular disease.
  • Hcy-thiolactone, an Hcy metabolite, is implicated in atherogenesis and thrombosis.
  • Hcy-thiolactone modifies proteins by forming isopeptide bonds with lysine residues.

Purpose of the Study:

  • To review evidence linking Hcy-thiolactone to the pathophysiological effects of Hcy.
  • To explore the role of protein N-homocysteinylation in vascular disease development.

Main Methods:

  • Review of existing scientific literature on Hcy-thiolactone and its effects.
  • Analysis of studies investigating protein modification by Hcy-thiolactone.
  • Examination of pathophysiological responses to N-homocysteinylated proteins.

Main Results:

  • Hcy-thiolactone is elevated in hyperhomocysteinemia.
  • Key blood proteins like fibrinogen, LDL, and HDL are targets for Hcy-thiolactone modification.
  • N-homocysteinylation of proteins contributes to thrombogenesis and autoimmune responses.

Conclusions:

  • Hcy-thiolactone's modification of proteins is a key mechanism driving vascular pathology.
  • Chronic N-homocysteinylation may lead to long-term vascular disease in hyperhomocysteinemia.
  • Hcy-thiolactone is a significant contributor to the vascular effects of homocysteine.

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