Cardiac hypertrophy: sorting out the circuitry.
Cardiac hypertrophy is an adaptive response of the heart to a variety of intrinsic and extrinsic stimuli. The hypertrophic response, during which cardiomyocytes increase in size without undergoing cell division, initially serves to compensate for decreased cardiac output; however, prolonged hypertrophy can become detrimental, resulting in dilated cardiomyopathy and heart failure. Cardiac hypertrophy requires coupling of intracellular signal transduction systems with transcription factors that activate and maintain the hypertrophic program. Over the past year, signaling pathways involving G proteins, mitogen-activated protein kinases and calcium-responsive phosphatases have emerged as critical regulators of cardiac hypertrophy.
McKinsey
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Department of Molecular Biology and Oncology University of Texas Southwestern Medical Center at Dallas, 75235-9148, USA.
Olson
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D000818:Animals; D019703:Calcineurin / Q000378:metabolism; D065095:Calcineurin Inhibitors; D006332:Cardiomegaly / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D016572:Cyclosporine / Q000494:pharmacology; D004268:DNA-Binding Proteins / Q000378:metabolism; D006801:Humans; D020935:MAP Kinase Signaling System; D050778:NFATC Transcription Factors; D009687:Nuclear Proteins; D014157:Transcription Factors / Q000378:metabolism
D065095:Calcineurin Inhibitors; D004268:DNA-Binding Proteins; D050778:NFATC Transcription Factors; D009687:Nuclear Proteins; D014157:Transcription Factors; D016572:Cyclosporine; D019703:Calcineurin