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Updated: Jul 4, 2026
Quantification of Atherosclerosis in Mice
Published on: June 12, 2019
Murine models of hyperhomocysteinemia and their vascular phenotypes
Sanjana Dayal1, Steven R Lentz
1Department of Internal Medicine, University of Iowa Carver College of Medicine, Iowa City, USA.
Insights
Severe hyperhomocysteinemia significantly increases vascular thrombosis risk. Murine models, including cystathionine beta-synthase deficient mice, are crucial for studying hyperhomocysteinemia
Area of Science:
- Cardiovascular Biology
- Metabolic Disorders
- Thrombosis Research
Background:
- Hyperhomocysteinemia is a known risk factor for arterial and venous thromboembolism.
- Severe genetic hyperhomocysteinemia leads to high vascular thrombosis rates without treatment.
- The role of homocysteine-lowering therapy in moderate hyperhomocysteinemia remains debated.
Purpose of the Study:
- To review established and novel murine models for studying hyperhomocysteinemia.
- To explore the vascular pathophysiology associated with elevated homocysteine levels.
- To summarize vascular phenotypes observed in hyperhomocysteinemia mouse models.
Main Methods:
- Utilizing genetic manipulations to induce hyperhomocysteinemia in mice (e.g., cystathionine beta-synthase deficiency).
- Employing dietary interventions to alter homocysteine metabolism and levels.
- Analyzing vascular phenotypes in various murine models of hyperhomocysteinemia.
Main Results:
- Murine models provide insights into the molecular mechanisms linking hyperhomocysteinemia and thrombosis.
- Cystathionine beta-synthase deficient mice are widely used to investigate vascular pathology.
- Various models allow for the study of induced hyperhomocysteinemia through genetic or dietary means.
Conclusions:
- Murine models are essential tools for understanding hyperhomocysteinemia's vascular consequences.
- These models facilitate research into the mechanisms of hyperhomocysteinemia-induced thrombosis.
- Reviewing these models aids in developing therapeutic strategies for vascular disease.
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.
