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Figure 6. Schematic representation of alternative intracellular pathways leading to myocardial hypertrophy.

Figure 6

Schematic representation of alternative intracellular pathways leading to myocardial hypertrophy. A large variety of physiological and pathological conditions are capable to induce cardiac hypertrophy by activating different membrane receptors and intracellular signaling pathways. As it can be appreciated several points of crosstalk between the intracellular pathways activated by G protein couple receptors (GPCR), receptors tyrosine kinase (RTyrK) and cytokine receptors exist; and all of them share the stimulation of the MAPK cascade. The three families of MAPK (ERK 1/2, p38MAPK and JNK) have been demonstrated to participate in the genesis of cardiac hypertrophy in different experimental models. They stimulate nuclear transcription factors and in the case of ERK 1/2 it has also been implicated in the activation of the NHE-1 through the p90rsk. An increase in [Ca2+]i leading to the activation of CaMKII and/or calcineurin, translocation to the nucleus of nuclear transcription factors and stimulation of gene transcription is shared by most of the intracellular pathways involved in the development of cardiac hypertrophy. From this schematic representation it becomes obvious that no single intracellular transduction cascade regulates cardiomyocyte hypertrophy in isolation, but instead each pathway operates as an integrated component of an orchestrated response.

From: The Na+/H+ Exchanger as the Main Protagonist following Myocardial Stretch: The Anrep Effect and Myocardial Hypertrophy

Cover of Mechanosensitivity in Cells and Tissues
Mechanosensitivity in Cells and Tissues.
Kamkin A, Kiseleva I, editors.
Moscow: Academia; 2005.
Copyright © 2005, Academia Publishing House Ltd.

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