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Models of Cardiac Disease in the Mouse

Cardiac Hypertrophy and Heart Failure

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Cardiovascular Physiology in the Genetically Engineered Mouse

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 238))

Abstract

Over the past decade the use of genetically engineered mouse models has led to considerable progress in understanding the pathophysiology of a variety of human diseases. Ability to manipulate the genome has allowed analysis of effects not only of gain or loss of the target gene function, but also actions of mutant alleles identified in human diseases. With regard to the cardiovascular system, although the mouse exhibits differences from humans in physiological variables and intracellular structure and function (e.g. isoforms of myosin heavy chain, relative contribution of sarcoplasmic reticulum (SR) to intracellular calcium regulation), a variety of approaches have been miniaturized for physiological studies in the mouse heart along with application to the mouse of methods for studying isolated cardiac muscle and cardiomyocytes. These approaches are listed in Table 19-1.

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Authors and Affiliations

  1. Division of Cardiology, Department of Medicine, University of California San Diego, La Jolla, CA, USA

    Yasuhiro Ikeda M.D., Ph.D. & John Ross Jr. M.D.

  2. Institute of Molecular Medicine, University of California San Diego, La Jolla, CA, USA

    John Ross Jr. M.D.

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  1. Yasuhiro Ikeda M.D., Ph.D.
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  2. John Ross Jr. M.D.
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Editors and Affiliations

  1. Case Western Reserve University and University Hospitals of Cleveland, USA

    Brian D. Hoit  & Richard A. Walsh  & 

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Ikeda, Y., Ross, J. (2001). Models of Cardiac Disease in the Mouse. In: Hoit, B.D., Walsh, R.A. (eds) Cardiovascular Physiology in the Genetically Engineered Mouse. Developments in Cardiovascular Medicine, vol 238. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1653-8_21

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