Mechanisms of homocysteine toxicity in humans

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

Research output: Contribution to journalReview article

201 Citations (Scopus)

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 1 2007

Fingerprint

Homocysteine
Toxicity
Proteins
Reticulum
Post Translational Protein Processing
Autoimmunity
Metabolism
Vasodilation
Amides
Disulfides
Endothelium
Myocardial Ischemia
Atherosclerosis
Stroke
Amino Acids

All Science Journal Classification (ASJC) codes

  • Endocrinology
  • Biochemistry
  • Clinical Biochemistry

Cite this

Perła-Kaján, J. ; Twardowski, T. ; Jakubowski, Hieronim. / Mechanisms of homocysteine toxicity in humans. In: Amino Acids. 2007 ; Vol. 32, No. 4. pp. 561-572.
@article{368f4795cf154668b9b5d0374e742c19,
title = "Mechanisms of homocysteine toxicity in humans",
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.",
author = "J. Perła-Kaj{\'a}n and T. Twardowski and Hieronim Jakubowski",
year = "2007",
month = "5",
day = "1",
doi = "https://doi.org/10.1007/s00726-006-0432-9",
language = "English (US)",
volume = "32",
pages = "561--572",
journal = "Amino Acids",
issn = "0939-4451",
publisher = "Springer Wien",
number = "4",

}

Mechanisms of homocysteine toxicity in humans. / Perła-Kaján, J.; Twardowski, T.; Jakubowski, Hieronim.

In: Amino Acids, Vol. 32, No. 4, 01.05.2007, p. 561-572.

Research output: Contribution to journalReview article

TY - JOUR

T1 - Mechanisms of homocysteine toxicity in humans

AU - Perła-Kaján, J.

AU - Twardowski, T.

AU - Jakubowski, Hieronim

PY - 2007/5/1

Y1 - 2007/5/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=34249086607&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34249086607&partnerID=8YFLogxK

U2 - https://doi.org/10.1007/s00726-006-0432-9

DO - https://doi.org/10.1007/s00726-006-0432-9

M3 - Review article

VL - 32

SP - 561

EP - 572

JO - Amino Acids

JF - Amino Acids

SN - 0939-4451

IS - 4

ER -