The Molecular and Cellular Effect of Homocysteine Metabolism Imbalance on Human Health

Homocysteine (Hcy) is a sulfur-containing non-proteinogenic amino acid derived in methionine metabolism. The increased level of Hcy in plasma, hyperhomocysteinemia, is considered to be an independent risk factor for cardio and cerebrovascular diseases. However, it is still not clear if Hcy is a mark...

Full description

Saved in:
Bibliographic Details
Published inInternational journal of molecular sciences Vol. 17; no. 10; p. 1733
Main Authors Škovierová, Henrieta, Vidomanová, Eva, Mahmood, Silvia, Sopková, Janka, Drgová, Anna, Červeňová, Tatiana, Halašová, Erika, Lehotský, Ján
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 20.10.2016
MDPI
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:Homocysteine (Hcy) is a sulfur-containing non-proteinogenic amino acid derived in methionine metabolism. The increased level of Hcy in plasma, hyperhomocysteinemia, is considered to be an independent risk factor for cardio and cerebrovascular diseases. However, it is still not clear if Hcy is a marker or a causative agent of diseases. More and more research data suggest that Hcy is an important indicator for overall health status. This review represents the current understanding of molecular mechanism of Hcy metabolism and its link to hyperhomocysteinemia-related pathologies in humans. The aberrant Hcy metabolism could lead to the redox imbalance and oxidative stress resulting in elevated protein, nucleic acid and carbohydrate oxidation and lipoperoxidation, products known to be involved in cytotoxicity. Additionally, we examine the role of Hcy in thiolation of proteins, which results in their molecular and functional modifications. We also highlight the relationship between the imbalance in Hcy metabolism and pathogenesis of diseases, such as cardiovascular diseases, neurological and psychiatric disorders, chronic kidney disease, bone tissue damages, gastrointestinal disorders, cancer, and congenital defects.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms17101733