Rabbit models of heart disease

Steven M. Pogwizd, Donald M Bers

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Human heart disease is a major cause of death and disability. A variety of animal models of cardiac disease have been developed to better understand the etiology, cellular and molecular mechanisms of cardiac dysfunction and novel therapeutic strategies. The animal models have included large animals (e.g. pig and dog) and small rodents (e.g. mouse and rat) and the advantages of genetic manipulation in mice have appropriately encouraged the development of novel mouse models of cardiac disease. However, there are major differences between rodent and human hearts that raise cautions about the extrapolation of results from mouse to human. The rabbit is a medium-sized animal that has many cellular and molecular characteristics very much like human, and is a practical alternative to larger mammals. Numerous rabbit models of cardiac disease are discussed, including pressure or volume overload, ischemia, rapid-pacing, doxorubicin, drug-induced arrhythmias, transgenesis and infection. These models also lead to the assessment of therapeutic strategies which may become beneficial in human cardiac disease.

Original languageEnglish (US)
Pages (from-to)185-193
Number of pages9
JournalDrug Discovery Today: Disease Models
Volume5
Issue number3
DOIs
StatePublished - Sep 2008

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Heart Diseases
Rabbits
Rodentia
Animal Models
Gene Transfer Techniques
Doxorubicin
Cardiac Arrhythmias
Cause of Death
Mammals
Swine
Ischemia
Dogs
Pressure
Therapeutics
Infection
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Drug Discovery
  • Molecular Medicine

Cite this

Rabbit models of heart disease. / Pogwizd, Steven M.; Bers, Donald M.

In: Drug Discovery Today: Disease Models, Vol. 5, No. 3, 09.2008, p. 185-193.

Research output: Contribution to journalArticle

Pogwizd, Steven M. ; Bers, Donald M. / Rabbit models of heart disease. In: Drug Discovery Today: Disease Models. 2008 ; Vol. 5, No. 3. pp. 185-193.
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