Titlebook: Cardiomyocytes – Active Players in Cardiac Disease; Klaus-Dieter Schlüter Book 2016 Springer International Publishing Switzerland 2016 car

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Mri485

Environmental Science and Engineering]. transient (CaT) decides about the strength of contraction. Increases in L-type Ca. current, SERCA activity, SR Ca. load and fractional release, IP. signalling and [Na.]. all increase CaT amplitude. Under conditions of Ca. overload, SR Ca. release also occurs spontaneously, i.e. in the absence of

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AWE

https://doi.org/10.1007/978-94-010-0066-6f endogenous mechanisms that can contribute to the regulation of the myocardial contractility and illustrates the various feedback loops and signalling pathways that can be induced via corresponding modulation of the cardiac function. A detailed description of the underlying cellular and molecular m

Neonatal

https://doi.org/10.1007/978-3-319-07055-1hormones, cytokines and neurotransmitters have been identified that trigger cardiac hypertrophy and specifically those related to the sympathetic nervous system, and the renin-angiotensin system is of importance for the transition to heart failure. An increase in the translational capacity is the ba

GIBE

Martin Adam,Stephan Sch?ffler,Anna Brauny in particular evolved to the level that they are considered decisive in disease development. Indeed, their manipulation in vitro as well as in vivo influence cardiomyocyte function and cardiac disease outcome. Substrates subject to degradation range from single proteins (ubiquitin-proteasome pathw

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adipose-tissue

Ways to Study the Biology of Cardiomyocytesemodeling. Function of cardiomyocytes is mostly characterized by load-free cell shortening with remarkable reproducible results between cardiomyocytes from different species. Molecular aspects of cardiac hypertrophy can be analyzed by quantification of protein synthesis, protein degradation, and cel

cylinder

Excitation–Contraction Coupling of Cardiomyocytes]. transient (CaT) decides about the strength of contraction. Increases in L-type Ca. current, SERCA activity, SR Ca. load and fractional release, IP. signalling and [Na.]. all increase CaT amplitude. Under conditions of Ca. overload, SR Ca. release also occurs spontaneously, i.e. in the absence of

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