Murine Models of Hyperhomocysteinemia and Their Vascular Phenotypes

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