MR in mouse models of cardiac disease.
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.
Epstein
Frederick H
FH
Departments of Radiology and Biomedical Engineering, and the Cardiovascular Research Center, University of Virginia, Charlottesville, VA 22908, USA. fredepstein@virginia.edu
D000818:Animals; D004195:Disease Models, Animal; D006331:Heart Diseases / Q000175:diagnosis* / Q000201:enzymology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D018810:Magnetic Resonance Angiography; D009682:Magnetic Resonance Spectroscopy; D051379:Mice; D009203:Myocardial Infarction / Q000503:physiopathology