Abstract
The influence of genetics in acquired adult heart disease remains incompletely defined. Genetic manipulation in mice has been widely used in combination with physiologic modeling to address this deficiency and has provided insights into the pathophysiology of myocardial signaling. However, conventional techniques of directed gene expression or ablation confound adult heart phenotypes with genetic perturbation of embryonic or postnatal cardiac development. Here, studies of Galphaq and Nix, powerful signaling factors for pathologic hypertrophy and cardiomyocyte apoptosis, respectively, are reviewed in terms of their comparative effects on cardiac development and adult cardiac pathology.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, P.H.S.
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Review
MeSH terms
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Animals
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Cardiomyopathies / genetics*
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Cardiomyopathies / physiopathology*
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Cardiomyopathy, Hypertrophic / genetics
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Cardiomyopathy, Hypertrophic / physiopathology
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GTP-Binding Protein alpha Subunits, Gq-G11 / metabolism*
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Heart / growth & development*
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Heart / physiopathology*
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Humans
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Membrane Proteins / metabolism*
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Mitochondrial Proteins / metabolism
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Proto-Oncogene Proteins / metabolism*
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Signal Transduction / genetics
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Tumor Suppressor Proteins / metabolism*
Substances
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BNIP3L protein, human
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BNIP3L protein, rat
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Membrane Proteins
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Mitochondrial Proteins
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Nix protein, mouse
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Proto-Oncogene Proteins
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Tumor Suppressor Proteins
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GTP-Binding Protein alpha Subunits, Gq-G11