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Biophysical Forces Modulate the Costamere and Z-Disc for Sarcomere Remodeling in Heart Failure

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Biophysics of the Failing Heart

Part of the book series: Biological and Medical Physics, Biomedical Engineering ((BIOMEDICAL))

Abstract

Cardiac remodeling at the macroscopic level occurs as the heart fails and is accompanied by changes in size, shape, and performance of its cardiomyocytes. Therefore, an understanding of the mechanisms by which cardiomyocytes sense and respond to biomechanical stress is of prime importance to the development of a molecular basis of heart failure. The cardiomyocyte experiences changes in stress and strain throughout every cardiac cycle, which is generated both internally by contractile proteins and externally through cell–cell and cell–matrix interactions. Cells within the heart are constantly remodeling through processes of gene transcription, protein translation, posttranslational modification, and the assembly of complex organelles. Because the heart is constantly challenged mechanically, it relies upon the near instantaneous posttranslational modifications of existing proteins to sense and respond rapidly to acute external stressors. Transcription and translation takes longer but are important to the overall response to chronic stress and strain. However, the mechanisms by which cardiomyocytes sense and respond to chronic mechanical strains remain largely unknown. Our team and many others are testing hypotheses that mechanical forces drive the growth of heart cells in healthy exercise but become maladaptive in disease. In this chapter we review how the biophysical forces in normal cardiomyocytes drive sarcomere remodeling in heart failure via two key structural components—namely the costamere at the cell membrane that is connected to the Z-disc of the myofibril. Each of these structural complexes has numerous proteins, many of which sense mechanical forces and are also involved in filament assembly. A diagram of the costamere and Z-disc indicates many of the key proteins (Fig. 1). In this chapter, we review how the costamere and specific components of the Z-disc may accomplish both functions of stress detection and sarcomere remodeling during adaptation to hemodynamic overload.

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Acknowledgments

Supported in part by NIH P01 HL62426, NIH 1F32 HL096143, and a grant from the Dr. Ralph and Marian Falk Medical Research Trust.

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  1. The Cardiovascular Institute, Stritch School of Medicine, Loyola University Chicago, Building 110, Room 5222, 2160 South First Avenue, Maywood, IL, 60153, USA

    Allen M. Samarel M.D. & Yevgeniya Koshman Ph.D.

  2. The Department of Physiology and Biophysics, University of Illinois—Chicago, Chicago, IL, 60612, USA

    Erik R. Swanson M.S. & Brenda Russell Ph.D.

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  1. Dept. of Physiology & Biophysics, University of Illinois at Chicago, Chicago, USA

    R. John Solaro

  2. University of Arizona, Tucson, Arizona, USA

    Jil C. Tardiff

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© 2013 Springer Science+Business Media, LLC

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Samarel, A.M., Koshman, Y., Swanson, E.R., Russell, B. (2013). Biophysical Forces Modulate the Costamere and Z-Disc for Sarcomere Remodeling in Heart Failure. In: Solaro, R., Tardiff, J. (eds) Biophysics of the Failing Heart. Biological and Medical Physics, Biomedical Engineering. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-7678-8_7

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