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Mitochondria in Cardiac Disease

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Translational Cardiology

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

Abstract

The heart has significant energy demands, and constant ATP generation is essential for the maintenance of cardiac function. Mitochondria are the cellular organelles that generate this ATP. In addition to this role, mitochondria contribute importantly to apoptotic cell death and to redox signaling. This chapter will provide an overview of the varied contributions of mitochondria to cardiac disease. We first review the basic machinery that converts metabolic energy to ATP via the process of oxidative phosphorylation (OXPHOS), and then review the processes that lead to the generation of mitochondrial reactive oxygen species (ROS) and the mechanisms by which ROS generation is regulated via activation of mitochondrial uncoupling proteins. The chapter reviews the mechanisms by which mitochondria can lead to cell death by activating apoptotic signaling and the role of the mitochondrial permeability transition pore in physiological states and in mediating oncotic cell death. These concepts are integrated in a discussion of ischemia-reperfusion injury. Mitochondria are dynamic organelles that undergo rapid turnover by processes such as mitophagy or by mitochondrial fusion and fission (a process known as mitochondrial dynamics). In addition, there are specific mechanisms by which new mitochondria are generated via a process known as mitochondrial biogenesis. Finally, altered mitochondrial function contributes to cardiac dysfunction in prevalent conditions such as diabetes and heart failure, and mechanisms leading to mitochondrial dysfunction in these circumstances are reviewed.

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Gottlieb, R.A., Quarato, G., Abel, E.D. (2012). Mitochondria in Cardiac 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_3

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