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Molecular Aspects of Mechanical Stress-Induced Cardiac Hypertrophy and Failure

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Book cover New Horizons for Failing Heart Syndrome

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Abstract

Studies have demonstrated that hypertensive left ventricular hypertrophy (LVH) simultaneously exhibits physiological and pathological aspects, suggesting that LVH is not a simple adaptation to an increased external load. Many investigators have extensively studied the activation of a novel program of gene expression in the heart induced by pressure overload (i.e., the transient induction of immediate early genes and the reexpression of fetal-type genes of both contractile and noncontractile proteins), which has been shown to be important as an adaptation to maintain cardiac function. Using an in vitro model system of mechanical stress-induced cardiac hypertrophy, we have demonstrated that the external stimuli imposed on cardiomyocytes are transduced into the nucleus through activation of the protein kinase cascade of phosphorylation: passive stretch of cultured cardiomyocytes stimulates the activation of protein kinase C, which leads to the successive phosphorylation of the mitogenactivated protein (MAP) kinase cascade including MAP kinase kinase kinase, MAP kinase, kinase, MAP kinase, and S6 kinase. Furthermore, we have demonstrated that the endogenous angiotensin II (Ang II) partially mediates mechanical stretch-induced cardiomyocyte hypertrophy, indicating that the cardiac tissue renin-angiotensin system plays an important role in the formation of hypertensive LVH. The precise mechanisms by which the sustained increase in external load leads to the impairment of cardiac function remain unclear, although impairment of diastolic function has been detected during the early stage of load-induced hypertrophy when there is no sign of reduced contractility. Using an in vivo model of hypertensive LVH, we noted previously that the depressed function of sarcoplasmic reticulum and the accumulation of interstitial collagen fibers may be responsible for the impaired diastolic function in stressed hearts. Here we review recent work on mechanical stress-induced cardiac hypertrophy and failure, especially bringing into focus the molecular mechanisms by which external load induces cellular hypertrophy of cardiac myocytes and impairment of the diastolic properties of the myocardium.

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Authors and Affiliations

  1. Department of Medicine III, University of Tokyo School of Medicine, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113, Japan

    Ichiro Shiojima, Tsutomu Yamazaki, Issei Komuro, Ryozo Nagai & Yoshio Yazaki

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  1. Ichiro Shiojima
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  2. Tsutomu Yamazaki
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  3. Issei Komuro
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  4. Ryozo Nagai
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  5. Yoshio Yazaki
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Editors and Affiliations

  1. Department of Cardiovascular Medicine, Kyoto University Graduate School of Medicine, 54 Shogoin Kawahara-cho, Sakyo-ku, Kyoto, 606, Japan

    Shigetake Sasayama M.D.

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© 1996 Springer Japan

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Shiojima, I., Yamazaki, T., Komuro, I., Nagai, R., Yazaki, Y. (1996). Molecular Aspects of Mechanical Stress-Induced Cardiac Hypertrophy and Failure. In: Sasayama, S. (eds) New Horizons for Failing Heart Syndrome. Springer, Tokyo. https://doi.org/10.1007/978-4-431-66945-6_1

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  • DOI: https://doi.org/10.1007/978-4-431-66945-6_1

  • Publisher Name: Springer, Tokyo

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