MR in mouse models of cardiac disease

Abstract

Transgenic and knockout mice can be used to study the genes and basic mechanisms involved in heart disease, and have therefore assumed a central role in modern cardiac research. MRI and MRS techniques have recently been developed for mice that enable the quantitative or semi-quantitative in vivo assessment of cardiac anatomy, function, perfusion, infarction, Ca(2+) influx, and metabolism. With these techniques, the normal mouse heart has been shown to be well suited as a model of human cardiac disease. The roles of individual genes in normal cardiac physiology have recently been studied by MR, including the role of neuronal nitric oxide synthase in beta-adrenergic stimulation, the roles of the inducible nitric oxide synthase and myoglobin in function, dilation, and energetics, and the role of cardiac troponin I in contractility. Furthermore, with a mouse model of myocardial infarction, the roles of the angiotensin II type 2 receptor, xanthine oxidase inhibitors, blood coagulation factor XIII, and inducible nitric oxide synthase in post-infarct function and remodeling have been further elucidated. Non-invasive in vivo MRI and MRS in mice provide a unique and powerful means for phenotyping genetically engineered mice and can improve our understanding of the roles of specific genes and proteins in cardiac physiology and pathophysiology.