ArticleArchives of physiology and biochemistry2011
Chronic hyperhomocysteinemia causes vascular remodelling by instigating vein phenotype in artery.
Article in Archives of physiology and biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Folic acid supplementation improves cognitive function in participants with cerebral small vascular disease-related cognitive impairment: a randomized controlled trial.The journal of prevention of Alzheimer's disease · 2026Trial
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- Review
- Effect of elastin-derived peptides on the production of tissue inhibitor of metalloproteinase-1, -2, and -3 and the ratios in various endothelial cell lines.Experimental and therapeutic medicine · 2015Article
- Dietary methionine restriction in mice elicits an adaptive cardiovascular response to hyperhomocysteinemia.Scientific reports · 2015Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
In the present study we tested the hypothesis whether hyperhomocysteinemia, an elevated homocysteine level, induces venous phenotype in artery. To test our hypothesis, we employed wild type (WT) and cystathionine β-synthase heterozygous (+/-) (CBS+/-) mice treatment with or without folic acid (FA). Aortic blood flow and velocity were significantly lower in CBS+/-mice compared to WT. Aortic lumen diameter was significantly decreased in CBS+/-mice, whereas FA treatment normalized it. Medial thickness and collagen were significantly increased in CBS+/-aorta, whereas elastin/collagen ratio was significantly decreased. Superoxide and gelatinase activity was significantly high in CBS+/-aorta vs WT. Western blot showed significant increase in MMP-2, -9,-12, TIMP-2 and decrease in TIMP-4 in aorta. RT-PCR revealed significant increase of vena cava marker EphB4, MMP-13 and TIMP-3 in aorta. We summarize that chronic HHcy causes vascular remodelling that transduces changes in vascular wall in a way that artery expresses vein phenotype.
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Registered trials
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