Abstract
Myosin is a molecular motor, which interacts with actin to convert the energy from ATP hydrolysis into mechanical work. In cardiac myocytes, two myosin isoforms are expressed and their relative distribution changes in different developmental and pathophysiologic conditions of the heart. It has been realized for a long time that a shift in myosin isoforms plays a major role in regulating myocardial contractile activity. With the recent evidence implicating that alteration in myosin isoform ratio may be eventually beneficial for the treatment of a stressed heart, a new interest has developed to find out ways of controlling the myosin isoform shift. This article reviews the published data describing the role of myosin isoforms in the heart and highlighting the importance of various factors shown to influence myosin isofrom shift during physiology and disease states of the heart.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Adrenergic beta-Antagonists / pharmacology
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Animals
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Cardiac Myosins / genetics*
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Cardiac Myosins / metabolism
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Cardiac Myosins / physiology
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Cardiomegaly / enzymology
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Cardiomegaly / etiology
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Cardiomegaly / genetics*
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Cardiomegaly / metabolism
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Chromatin Assembly and Disassembly / genetics
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Diabetes Complications / metabolism
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Diabetes Mellitus / metabolism
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Gene Expression Regulation / drug effects
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Heart Failure / enzymology
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Heart Failure / etiology
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Heart Failure / genetics*
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Heart Failure / metabolism
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Humans
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MicroRNAs / physiology
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Models, Biological
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Myosin Heavy Chains / genetics
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Protein Isoforms / genetics
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Protein Isoforms / metabolism
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Receptors, Adrenergic, beta / physiology
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Thyroid Hormones / pharmacology
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Tissue Distribution
Substances
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Adrenergic beta-Antagonists
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MicroRNAs
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Protein Isoforms
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Receptors, Adrenergic, beta
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Thyroid Hormones
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Cardiac Myosins
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Myosin Heavy Chains