Murine models of hyperhomocysteinemia and their vascular phenotypes

Sanjana Dayal; Steven R Lentz

doi:10.1161/ATVBAHA.108.166421

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Murine models of hyperhomocysteinemia and their vascular phenotypes

Journal article

Open access

Peer reviewed

Murine models of hyperhomocysteinemia and their vascular phenotypes

Sanjana Dayal and Steven R Lentz

Arteriosclerosis, thrombosis, and vascular biology, Vol.28(9), pp.1596-1605

09/2008

DOI: 10.1161/ATVBAHA.108.166421

PMCID: PMC2574668

PMID: 18556571

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https://doi.org/10.1161/ATVBAHA.108.166421View

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Abstract

Hyperhomocysteinemia is an established risk factor for arterial as well as venous thromboembolism. Individuals with severe hyperhomocysteinemia caused by inherited genetic defects in homocysteine metabolism have an extremely high incidence of vascular thrombosis unless they are treated aggressively with homocysteine-lowering therapy. The clinical value of homocysteine-lowering therapy in individuals with moderate hyperhomocysteinemia, which is very common in populations at risk for vascular disease, is more controversial. Considerable progress in our understanding of the molecular mechanisms underlying the association between hyperhomocysteinemia and vascular thrombotic events has been provided by the development of a variety of murine models. Because levels of homocysteine are regulated by both the methionine and folate cycles, hyperhomocysteinemia can be induced in mice through both genetic and dietary manipulations. Mice deficient in the cystathionine beta-synthase (CBS) gene have been exploited widely in many studies investigating the vascular pathophysiology of hyperhomocysteinemia. In this article, we review the established murine models, including the CBS-deficient mouse as well as several newer murine models available for the study of hyperhomocysteinemia. We also summarize the major vascular phenotypes observed in these murine models.

Enzyme Inhibitors - adverse effects

Genetic Predisposition to Disease

Thrombosis - physiopathology

Diet - adverse effects

Endothelium, Vascular - physiopathology

Hyperhomocysteinemia - metabolism

Homocysteine - metabolism

Hyperhomocysteinemia - etiology

Hyperhomocysteinemia - physiopathology

Phenotype

Thrombosis - metabolism

Animals

Endothelium, Vascular - metabolism

Thrombosis - etiology

Betaine-Homocysteine S-Methyltransferase - antagonists & inhibitors

Mice

Betaine-Homocysteine S-Methyltransferase - metabolism

Hyperhomocysteinemia - complications

Disease Models, Animal

Details

Title: Subtitle: Murine models of hyperhomocysteinemia and their vascular phenotypes
Creators: Sanjana Dayal - Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, USA
Steven R Lentz
Resource Type: Journal article
Publication Details: Arteriosclerosis, thrombosis, and vascular biology, Vol.28(9), pp.1596-1605
DOI: 10.1161/ATVBAHA.108.166421
PMID: 18556571
PMCID: PMC2574668
NLM abbreviation: Arterioscler Thromb Vasc Biol
ISSN: 1079-5642
eISSN: 1524-4636
Publisher: United States
Grant note: NS24621 / NINDS NIH HHS R01 HL063943 / NHLBI NIH HHS P01 NS024621 / NINDS NIH HHS R01 HL063943-08 / NHLBI NIH HHS HL63943 / NHLBI NIH HHS P01 NS024621-21A15447 / NINDS NIH HHS
Language: English
Date published: 09/2008
Academic Unit: Hematology, Oncology, and Blood & Marrow Transplantation; Iowa Neuroscience Institute; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
Record Identifier: 9984065383102771

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