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Identifying the Cellular and Molecular Events Associated with the Divergent Phenotypes of Cardiac Hypertrophy

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Part of the book series: Advances in Biochemistry in Health and Disease ((ABHD,volume 3))

Abstract

Following the imposition of a hemodynamic load, the primary adaptive response of the heart involves an increase in size of individual cardiac myocytes in the absence of cell division. This process is characterized as cardiac hypertrophy and the pattern of individual myocyte growth is directly influenced by the nature of the hemodynamic load. Cardiac hypertrophy can be classified as either physiological or pathological and their disparate phenotypes are related in part to a divergent pattern of peptide growth factor expression. Gq-mediated recruitment of Ca2+- and PKC-dependent signaling pathways may primarily be implicated in the progression of pathological hypertrophy characterized by a concentric pattern of remodeling. By contrast, recruitment of the phosphatidylinositol 3-kinase isoform p110α may selectively participate in the physiological growth of cardiac myocytes. However, there exists evidence to suggest that Ca2+-dependent pathways may also play a supporting role in physiological cardiac hypertrophy. Thus, this review will provide a comprehensive analysis of the morphological, cellular, and molecular phenotypes of physiological and pathological cardiac hypertrophy and explore the relative contribution of Gq- and phosphatidylinositol 3-kinase-dependent pathways.

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Calderone, A. (2008). Identifying the Cellular and Molecular Events Associated with the Divergent Phenotypes of Cardiac Hypertrophy. In: Srivastava, A.K., Anand-Srivastava, M.B. (eds) Signal Transduction in the Cardiovascular System in Health and Disease. Advances in Biochemistry in Health and Disease, vol 3. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-09552-3_12

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