Physiologic growth and pathologic genes in cardiac development and cardiomyopathy.
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.
Dorn
Gerald W
GW
Department of Molecular Genetics, Biochemistry and Microbiology, University of Cincinnati, 231 Albert Sabin Lane, Cincinnati, OH 45267-0542, USA. gerald.dorn@uc.edu
D000818:Animals; D009202:Cardiomyopathies / Q000235:genetics* / Q000503:physiopathology*; D002312:Cardiomyopathy, Hypertrophic / Q000235:genetics / Q000503:physiopathology; D043802:GTP-Binding Protein alpha Subunits, Gq-G11 / Q000378:metabolism*; D006321:Heart / Q000254:growth & development* / Q000503:physiopathology*; D006801:Humans; D008565:Membrane Proteins / Q000378:metabolism*; D024101:Mitochondrial Proteins / Q000378:metabolism; D011518:Proto-Oncogene Proteins / Q000378:metabolism*; D015398:Signal Transduction / Q000235:genetics; D025521:Tumor Suppressor Proteins / Q000378:metabolism*
C116838:BNIP3L protein, human; C505659:BNIP3L protein, rat; D008565:Membrane Proteins; D024101:Mitochondrial Proteins; C501741:Nix protein, mouse; D011518:Proto-Oncogene Proteins; D025521:Tumor Suppressor Proteins; D043802:GTP-Binding Protein alpha Subunits, Gq-G11