Format

Send to:

Choose Destination
See comment in PubMed Commons below
J Inherit Metab Dis. 1997 Jun;20(2):307-15.

Putative mechanisms for vascular damage by homocysteine.

Author information

  • 1Cardiovascular Sciences Research Group, University of Wales College of Medicine, Cardiff, UK.

Abstract

In homocystinuria homocysteine appears to be directly toxic to the vasculature, but in mild hyperhomocysteinaemia a cause and effect relationship remains unproven. Evidence for a causal role is derived from recent primate and human studies in which endothelial dysfunction was produced by modestly elevated blood homocysteine concentrations. Endothelial dysfunction would account for an increased risk of both arterial and venous disease. A key abnormality may be impaired release and/or action of nitric oxide in response to flow. Other possible mechanisms include smooth muscle cell proliferation, extracellular matrix modification and lipoprotein oxidation. Although demonstrated in vitro, a role for lipoprotein oxidation in man has not been substantiated. However an effect of homocysteine on cellular redox status remains a possible mechanism. Homocysteine does not appear to alter circulating coagulation factors consistently, but may promote enhanced thrombin production indirectly by its effects on endothelium. Further studies are required to elucidate the pathological actions of homocysteine, concentrating on the effects of mild hyper-homocysteinaemia on endothelial function in man.

PMID:
9211203
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Loading ...
    Write to the Help Desk