Abstract
All cells in multi-cellular organisms must be able to sense their surrounding environment and and respond based upon this information. In a similar fashion, cardiac muscle cells are equipped with a specialized protein machinery composed of detection systems (receptors), intermediate proteins within the cell for information transduction (intracellular signal transducers) and nuclear components specialized in changing the genetic profile of the cell (transcription factors). This integrated system is the subject of part of the biological sciences that studies “signal transduction” or shortly “signaling”, and topics the molecular mechanisms by which transfer of biological - information at the cellular level is converted. Cardiac signaling systems provide crucial information for cells to decide about differentiation status, death or metabolic control. As such, it is not surprising that many signaling malfunctions underly human diseases. For example, cancer evolves following inactivating mutations in growth-inhibitory pathways, resulting in specialized cells with proliferative advantages over its neighbouring cells[1]. Diabetes results from defects in the insulin-signaling pathway used to control blood glucose levels[2]. Certain forms of achrondoplasia (dwarfism) result from mutations in the receptor tyrosine kinase for fibroblast growth factor, [3] while in agammaglobulinaemia (failure to produce immunoglobulins in the blood), a mutation in the B-cell tyrosine kinase Btk results in a failure of this enzyme to respond to activation of the enzyme phosphatidylinositol-3-OH kinase (PI-3K) [4].
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Bueno, O.F., van Rooij, E., Lips, D.J., Doevendans, P.A., De Windt, L.J. (2002). Cardiac Hypertrophic Signaling the Good, the Bad and the Ugly. In: Doevendans, P.A., Kääb, S. (eds) Cardiovascular Genomics: New Pathophysiological Concepts. Developments in Cardiovascular Medicine, vol 242. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1005-5_13
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DOI: https://doi.org/10.1007/978-1-4615-1005-5_13
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