Heart failure is a leading cause of mortality in the UnitedStates. As a result of advances in genetic technology, a molecularbasis of heart failure is emerging.1,2 This review highlightsthe ways in which these insights are leading to new therapeutictargets in patients with acquired forms of heart failure.
Morphologic Classification of Cardiac Hypertrophy
Myocardial hypertrophy is an early milestone during the clinicalcourse of heart failure and an important risk factor for subsequentcardiac morbidity and mortality. In response to a variety ofmechanical, hemodynamic, hormonal, and pathologic stimuli, theheart adapts to increased demands for cardiac work by increasingmuscle mass . . . [Full Text of this Article]
Genetic Methods of Studying Cardiac Hypertrophy and Failure
Assays of Cardiac-Muscle Cells
Cardiac Hypertrophy and Failure in Genetically Altered Animals
Pressure Overload and Concentric Hypertrophy
Chamber Dilatation and Dilated Cardiomyopathy
Apoptosis of Cardiac Myocytes
Cardiac Function and Contractility
Conclusions
Source Information
From the University of California San Diego–Salk Institute Program in Molecular Medicine, Department of Medicine and Center for Molecular Genetics, University of California San Diego School of Medicine, La Jolla, Calif.
Address reprint requests to Dr. Chien at the Department of Medicine, 0613-C, University of California San Diego, 9500 Gilman Dr., La Jolla, CA 92093, or at kchien@ucsd.edu.
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Ancey, C., Menet, E., Corbi, P., Fredj, S., Garcia, M., Rucker-Martin, C., Bescond, J., Morel, F., Wijdenes, J., Lecron, J.-C., Potreau, D.
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(2003). Cocaine Produces Cardiac Hypertrophy by Protein Kinase C Dependent Mechanisms. J CARDIOVASC PHARMACOL THER
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(2003). Clinical implications of apoptosis in hypertensive heart disease. Am. J. Physiol. Heart Circ. Physiol.
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(2003). New heart failure therapy: The shape of things to come?. J. Thorac. Cardiovasc. Surg.
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(2003). Alterations in Janus Kinase (JAK)-Signal Transducers and Activators of Transcription (STAT) Signaling in Patients With End-Stage Dilated Cardiomyopathy. Circulation
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Wang, X., Ren, B., Liu, S., Sentex, E., Tappia, P. S., Dhalla, N. S.
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Pikkarainen, S., Tokola, H., Kerkela, R., Majalahti-Palviainen, T., Vuolteenaho, O., Ruskoaho, H.
(2003). Endothelin-1-specific Activation of B-type Natriuretic Peptide Gene via p38 Mitogen-activated Protein Kinase and Nuclear ETS Factors. J. Biol. Chem.
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Steenman, M., Chen, Y.-W., Le Cunff, M., Lamirault, G., Varro, A., Hoffman, E., Leger, J. J.
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van Rooij, E., Doevendans, P. A., de Theije, C. C., Babiker, F. A., Molkentin, J. D., De Windt, L. J.
(2002). Requirement of Nuclear Factor of Activated T-cells in Calcineurin-mediated Cardiomyocyte Hypertrophy. J. Biol. Chem.
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BEHFAR, A., ZINGMAN, L. V., HODGSON, D. M., RAUZIER, J.-M., KANE, G. C., TERZIC, A., PUCEAT, M.
(2002). Stem cell differentiation requires a paracrine pathway in the heart. FASEB J.
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Chaqour, B., Whitbeck, C., Han, J.-S., Macarak, E., Horan, P., Chichester, P., Levin, R.
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Erami, C., Zhang, H., Ho, J. G., French, D. M., Faber, J. E.
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Fiedler, B., Lohmann, S. M., Smolenski, A., Linnemuller, S., Pieske, B., Schroder, F., Molkentin, J. D., Drexler, H., Wollert, K. C.
(2002). Inhibition of calcineurin-NFAT hypertrophy signaling by cGMP-dependent protein kinase type I in cardiac myocytes. Proc. Natl. Acad. Sci. USA
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Black, R. G. Jr, Guo, Y., Ge, Z.-D., Murphree, S. S., Prabhu, S. D., Jones, W. K., Bolli, R., Auchampach, J. A.
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