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Cardiac Plasticity in Health and Disease

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Translational Cardiology

Part of the book series: Molecular and Translational Medicine ((MOLEMED))

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Abstract

The heart is a remarkably plastic organ. In the setting of disease-related stress, such as unremitting hypertension or myocardial injury, hypertrophic growth takes place that increases the risk of functional decompensation and malignant rhythm disturbance. However, not all hypertrophy is pathological; growth of the heart into the setting of physiological demand is adaptive and is not associated with adverse sequelae. The heart can also diminish in size. Indeed, it is capable of shrinking up to 25% under a variety of clinically relevant circumstances, such as ventricular unloading by means of bedrest, mechanical support, or weightlessness. Each of these major forms of myocardial plasticity is associated with energy-dependent remodeling of the major components of the myocyte, coordinated angiogenic alterations in blood supply, adjustments in the consumption of energy-providing substrates, and, in the cases of pathological hypertrophy and myocyte atrophy, activation of a previously dormant “fetal gene program.” Here, we review mechanisms whereby the myocardium increases or decreases in size, the relevance of these mechanisms to normal physiology and cardiovascular disease, and the prospects for targeting these processes for therapeutic gain.

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Acknowledgments

We thank members of the Hill and Rothermel laboratories for thoughtful commentary. This work was supported by grants from the NIH (HL-075173, JAH; HL-080144, JAH; HL-090842, JAH; HL-072016, BAR; HL-097768, BAR), AHA (0640084N, JAH; 0655202Y, BAR), ADA (7-08-MN-21-ADA, JAH), and the AHA-Jon Holden DeHaan Foundation (0970518N, JAH).

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  1. Division of Cardiology, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX, 75390 8573, USA

    Raj B. Gondalia, Beverly A. Rothermel, Thomas G. Gillette & Joseph A. Hill

  2. Division of Cardiology, UT Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX, 75390-8573, USA

    Sergio Lavandero

  3. Center for Molecular Studies of the Cell, University of Chile, Santiago, RM, Chile

    Sergio Lavandero

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  1. Raj B. Gondalia
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  2. Beverly A. Rothermel
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  5. Joseph A. Hill
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Correspondence to Joseph A. Hill .

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Editors and Affiliations

  1. , The University of North Carolina, McAllister Heart Institute, 6022 - Burnett Womack Building, Chapel Hill, 27599-7075, North Carolina, USA

    Cam Patterson

  2. , The University of North Carolina, McAllister Heart Institute, 103 Mason Farm Road, Chapel Hill, 27599-7525, USA

    Monte S. Willis

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Gondalia, R.B., Rothermel, B.A., Lavandero, S., Gillette, T.G., Hill, J.A. (2012). Cardiac Plasticity in Health and Disease. In: Patterson, C., Willis, M. (eds) Translational Cardiology. Molecular and Translational Medicine. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-61779-891-7_7

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