Chapter Category: Heart

From the book Cardiac Mechanotransduction

Intracellular Signaling Through Protein Kinases in Cardiac Mechanotransduction

Peter H. Sugden

There is good evidence that stress-induced deformation of the cardiac myocyte can activate intracellular signaling pathways, though how this is brought about is still partly a mystery, some clues being provided by the present volume of reviews. The activation of these signaling pathways is thought to be instrumental in producing the changes in myocyte morphology, sarcomerogenesis, and gene expression that occur during hypertrophic growth. Reversible protein phosphorylation and dephosphosphorylation control a wide range biological responses, and hypertrophic growth is no exception. Specifically, there is evidence of a role for lipid-based signaling and protein kinase C in strain-induced signaling events. Activation of protein kinase C is probably instrumental in activating the extracellular signal-regulated kinase 1/2 cascade. However, other protein kinases are activated by strain: these included stress-activated protein kinases (c-Jun N-terminal kinases, p38-mitogen-activated protein kinases) and the Janus activated kinases. Apart from these, there is also evidence that the extracellular matrix, focal adhesion-based signaling and activation of the focal adhesion kinase may play a role in the response of myocytes to strain. The myocyte probably integrates the myriad messages from a variety of signaling pathways and this determines the overall biological response.

Taken from the book

Cardiac Mechanotransduction

Edited by: Matti Weckstrom and Pasi Tavi

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