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Mitochondrial Fission and Autophagy in the Normal and Diseased Heart

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Abstract

Sustained hypertension promotes structural, functional and metabolic remodeling of cardiomyocyte mitochondria. As long-lived, postmitotic cells, cardiomyocytes turn over mitochondria continuously to compensate for changes in energy demands and to remove damaged organelles. This process involves fusion and fission of existing mitochondria to generate new organelles and separate old ones for degradation via autophagy. Autophagy is a lysosome-dependent proteolytic pathway capable of processing cellular components, including organelles and protein aggregates. Autophagy can be either nonselective or selective and contributes to remodeling of the myocardium under stress. Fission of mitochondria, loss of membrane potential, and ubiquitination are emerging as critical steps that direct selective autophagic degradation of mitochondria. This review discusses the molecular mechanisms controlling mitochondrial dynamics, including fission, fusion, transport, and degradation. Furthermore, it examines recent studies revealing the importance of these processes in normal and diseased heart.

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Acknowledgments

This research was funded in part by the National Institutes of Health (to J.A.H. and B.A.R.), the American Heart Association (to M.I., J.A.H., and B.A.R.), the American Heart Association-Jon Holden DeHaan Foundation (to J.A.H.), FONDECYT 1080436 (to S.L.), and FONDAP 1501006 (to S.L).

We would like to thank Dr. Randy McMillan and Dr. Thomas Gillette for critical reading of this manuscript.

Disclosure

No potential conflicts of interest relevant to this article were reported.

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Authors and Affiliations

  1. Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, TX, 75390-8573, USA

    Beverly A. Rothermel

  2. Department of Internal Medicine (Cardiology), University of Texas Southwestern Medical Center, Dallas, TX, 75390-8573, USA

    Myriam Iglewski, Joseph A. Hill & Sergio Lavandero

  3. Departments of Internal Medicine (Cardiology) and Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, 75390-8573, USA

    Joseph A. Hill

  4. Centro Estudios Moleculares de la Célula, Facultad de Ciencias Químicas y Farmacéuticas & Facultad de Medicina, Universidad de Chile, Santiago, 838-0492, Chile

    Sergio Lavandero

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  1. Myriam Iglewski
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  4. Beverly A. Rothermel
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Correspondence to Beverly A. Rothermel.

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Iglewski, M., Hill, J.A., Lavandero, S. et al. Mitochondrial Fission and Autophagy in the Normal and Diseased Heart. Curr Hypertens Rep 12, 418–425 (2010). https://doi.org/10.1007/s11906-010-0147-x

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  • DOI: https://doi.org/10.1007/s11906-010-0147-x

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