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Mitochondria, Myocardial Remodeling, and Cardiovascular Disease

  • Mediators, Mechanisms, and Pathways in Tissue Injury (B Rothermel, Section Editor)
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Abstract

The process of muscle remodeling lies at the core of most cardiovascular diseases. Cardiac adaptation to pressure or volume overload is associated with a complex molecular change in cardiomyocytes which leads to anatomic remodeling of the heart muscle. Although adaptive at its beginnings, the sustained cardiac hypertrophic remodeling almost unavoidably ends in progressive muscle dysfunction, heart failure and ultimately death. One of the features of cardiac remodeling is a progressive impairment in mitochondrial function. The heart has the highest oxygen uptake in the human body and accordingly it has a large number of mitochondria, which form a complex network under constant remodeling in order to sustain the high metabolic rate of cardiac cells and serve as Ca2+ buffers acting together with the endoplasmic reticulum (ER). However, this high dependence on mitochondrial metabolism has its costs: when oxygen supply is threatened, high leak of electrons from the electron transport chain leads to oxidative stress and mitochondrial failure. These three aspects of mitochondrial function (Reactive oxygen species signaling, Ca2+ handling and mitochondrial dynamics) are critical for normal muscle homeostasis. In this article, we will review the latest evidence linking mitochondrial morphology and function with the process of myocardial remodeling and cardiovascular disease.

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Acknowledgments

This research was funded in part by Comision Nacional de Ciencia y Tecnologia (CONICYT), Chile: Fondo Desarrollo en Areas Prioritarias 15010006 (S.L.), Anillo de Investigación de Ciencia y Tecnología ACT1111 (S.L., P.F.C., L.G.), FONDECYT 1120212 (S.L.), FONDECYT 1090727 (P.F.C.), FONDECYT 3110114 (R.T.), FONDECYT 3110039 (Z.P.) and FONDECYT 3120220 (C.Q.). We thank the PhD fellowships from MECESUP and CONICYT, Chile to H.E.V., and A.d.C, respectively.

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Authors and Affiliations

  1. Centro Estudios Moleculares de la Célula, Facultad Ciencias Químicas y Farmacéuticas/Facultad de Medicina, Universidad de Chile, Olivos 1007, Santiago, 8380492, Chile

    Hugo E. Verdejo, Andrea del Campo, Rodrigo Troncoso, Tomás Gutierrez, Barbra Toro, Clara Quiroga, Zully Pedrozo, Lorena Garcia & Sergio Lavandero

  2. Division de Enfermedades Cardiovasculares. Facultad de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile

    Hugo E. Verdejo & Pablo F. Castro

  3. Institute for Research in Biomedicine, Barcelona, 08028, Spain

    Juan Pablo Munoz

  4. Department of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, Texas, 75235, USA

    Sergio Lavandero

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  1. Hugo E. Verdejo
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  2. Andrea del Campo
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  3. Rodrigo Troncoso
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  11. Sergio Lavandero
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Correspondence to Sergio Lavandero.

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Verdejo, H.E., del Campo, A., Troncoso, R. et al. Mitochondria, Myocardial Remodeling, and Cardiovascular Disease. Curr Hypertens Rep 14, 532–539 (2012). https://doi.org/10.1007/s11906-012-0305-4

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