Mechanisms of homocysteine toxicity in humans

J. Perła-Kaján, T. Twardowski, H. Jakubowski

Research output: Contribution to journalReview articlepeer-review

272 Scopus citations

Abstract

Homocysteine, a non-protein amino acid, is an important risk factor for ischemic heart disease and stroke in humans. This review provides an overview of homocysteine influence on endothelium function as well as on protein metabolism with a special respect to posttranslational modification of protein with homocysteine thiolactone. Homocysteine is a pro-thrombotic factor, vasodilation impairing agent, pro-inflammatory factor and endoplasmatic reticulum-stress inducer. Incorporation of Hcy into protein via disulfide or amide linkages (S-homocysteinylation or N-homocysteinylation) affects protein structure and function. Protein N-homocysteinylation causes cellular toxicity and elicits autoimmune response, which may contribute to atherogenesis.

Original languageEnglish (US)
Pages (from-to)561-572
Number of pages12
JournalAmino Acids
Volume32
Issue number4
DOIs
StatePublished - May 2007

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Organic Chemistry
  • Clinical Biochemistry

Keywords

  • Autoantibodies
  • Homocysteine
  • Homocysteine thiolactone
  • Protein N-homocysteinylation
  • Protein S-homocysteinylation
  • Toxicity

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