Cardiac physiology in transgenic mice. Circ Res 1998 Mar 09;82(4):407-15
Date
03/20/1998Pubmed ID
9506700DOI
10.1161/01.res.82.4.407Scopus ID
2-s2.0-0032498785 (requires institutional sign-in at Scopus site) 157 CitationsAbstract
By use of gene targeting and/or transgenesis, it is now possible to make defined changes in genes whose functions underlie mammalian cardiovascular function. Because of technical and economic considerations, these experiments are largely confined to the mouse. Genetic modification of the loci responsible for aspects of cardiac development, differentiation, and function via gene targeting, as well as modulation of the cardiac protein complement using transgenesis, has begun to provide mouse models of cardiac hypertrophy, dilated cardiomyopathy, and hypertrophic cardiomyopathies. In order to use these animal models fully and explore their phenotypes at the whole organ and whole animal levels, the extension of cardiovascular physiological methodologies to the mouse is imperative. Techniques for exploring aspects of cardiovascular function are well developed for larger animal models, but their modification for the small size of the mouse heart and for the animal's rapid cardiac cycle has proven to be a formidable challenge, requiring the combined efforts of the molecular biology, physiology, and cardiology communities. We review here the ability of present-day technology to obtain reproducible data on murine cardiac function at the whole organ and animal levels.
Author List
James JF, Hewett TE, Robbins JMESH terms used to index this publication - Major topics in bold
AnimalsBlood Pressure
Disease Models, Animal
Electrophysiology
Heart
Heart Diseases
Magnetic Resonance Imaging
Methods
Mice
Mice, Transgenic
Perfusion
Physical Exertion
