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Signal Transduction in Myocardial Hypertrophy and Myosin Expression

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Book cover Subcellular Basis of Contractile Failure

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 116))

Abstract

Myocardial hypertrophy is associated with a number of heart diseases and is of great clinical relevance. Despite many research efforts, the signals involved in the hypertrophy process are still poorly understood (1–4). Recently, it was found that the subcellular structure of the myocyte differs in various forms of hypertrophy. Great emphasis has been placed on gene expression of the myosin heavy chains (MHC) which determine the isoenzyme population of myosin. The myosin isoenzymes influence the ATPase activity (5,6), the energetics of the cross bridge cycle (7,8), oxygen consumption of the whole heart (9,10) and the mechanics of heart muscle (11–13). Although changes in the MHC expression are less relevant for the heart of large mammals with predominantly V3, they nonetheless provide the unique possibility of tracing an altered mechanical performance of the heart to an altered gene expression. Because there is increasing evidence that in a number of functional states the MHC expression is associated with coordinated changes in the activity of the Ca2+-stimulated ATPase of sarcoplasmic reticulum (14,15), a better understanding of the regulation of gene expression of myosin should help also in understanding the regulation of the activity of the sarcoplasmic reticulum Ca2+-pump.

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Borivoj Korecky Naranjan S. Dhalla

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© 1990 Kluwer Academic Publishers

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Rupp, H., Jacob, R., Dhalla, N.S. (1990). Signal Transduction in Myocardial Hypertrophy and Myosin Expression. In: Korecky, B., Dhalla, N.S. (eds) Subcellular Basis of Contractile Failure. Developments in Cardiovascular Medicine, vol 116. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1513-1_9

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  • DOI: https://doi.org/10.1007/978-1-4613-1513-1_9

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4612-8813-8

  • Online ISBN: 978-1-4613-1513-1

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