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Homocysteine in myointimal hyperplasia
M Hansrani1, J I Gillespie, G Stansby
1Department of Surgery, University of Newcastle upon Tyne, Newcastle upon Tyne, UK.
Insights
Homocysteine
Area of Science:
- Cardiovascular Science
- Vascular Biology
- Biochemistry
Background:
- Homocysteine, a non-essential amino acid, is implicated in atherosclerosis.
- Its role in myointimal hyperplasia, a cause of interventional procedure failure, is less understood.
Purpose of the Study:
- To review existing scientific data on homocysteine's role in myointimal hyperplasia.
- To elucidate potential mechanisms of homocysteine's action on vascular tissue.
Main Methods:
- Comprehensive literature review using MEDLINE and other databases.
- Inclusion of evidence from cell culture, animal models, and clinical studies.
Main Results:
- Clinical studies show a link between plasma homocysteine and restenosis, but results are contradictory.
- Cell and animal studies suggest mechanisms involving endothelial cell activation and vascular smooth muscle cell proliferation.
- No randomized trials currently exist.
Conclusions:
- Further research is needed to clarify homocysteine's role in myointimal hyperplasia pathogenesis.
- If confirmed, homocysteine normalization presents a potential therapeutic target.
Introduction:
homocysteine, a sulphur-containing non-essential amino acid, appears to play a role in the pathophysiology of atherosclerosis. However, its role in myointimal hyperplasia, the cause of almost 30% of failures of interventional therapeutic procedures, is much less clear.
Methods:
a review of the published scientific data concerning the role of homocysteine in myointimal hyperplasia was performed using MEDLINE and other on-line databases. Evidence was sought from cell culture experiments, animal models and clinical studies.
Results:
several clinical studies have recently been published linking plasma homocysteine levels to restenosis in coronary and peripheral arterial disease. However, several contradictory studies also exist making the role of homocysteine unclear. There are currently no published randomised trials. Cell culture and animal model experiments have elucidated several potential mechanisms by which may stimulate myointimal hyperplasia. Possible mechanisms include endothelial cell activation with the enhanced release of inflammatory cytokines and growth factors and a direct effect on vascular smooth muscle cell migration and proliferation.
Conclusions:
further studies are required before the true role of homocysteine in the pathogenesis of myointimal hyperplasia can be clearly evaluated. If evidence does confirm a role, the ease with which homocysteine levels can be normalised makes it an attractive alternative therapeutic target for intervention.