Abstract
Mitochondria represent approximately one-third of the mass of the heart and play a critical role in maintaining cellular function- however, they are also a potent source of free radicals and pro-apoptotic factors. As such, maintaining mitochondrial homeostasis is essential to cell survival. As the dominant source of ATP, continuous quality control is mandatory to ensure their ongoing optimal function. Mitochondrial quality control is accomplished by the dynamic interplay of fusion, fission, autophagy, and mitochondrial biogenesis. This review examines these processes in the heart and considers their role in the context of ischemia-reperfusion injury. Interventions that modulate mitochondrial turnover, including pharmacologic agents, exercise, and caloric restriction are discussed as a means to improve mitochondrial quality control, ameliorate cardiovascular dysfunction, and enhance longevity.
Keywords: Autophagy, caloric restriction, cardioprotection, exercise, ischemia-reperfusion, mitochondria, mitochondrial turnover, preconditioning, glycolysis, mitophagy
Current Pharmaceutical Design
Title: Mitochondrial Therapeutics for Cardioprotection
Volume: 17 Issue: 20
Author(s): Raquel S. Carreira, Pamela Lee and Roberta A. Gottlieb
Affiliation:
Keywords: Autophagy, caloric restriction, cardioprotection, exercise, ischemia-reperfusion, mitochondria, mitochondrial turnover, preconditioning, glycolysis, mitophagy
Abstract: Mitochondria represent approximately one-third of the mass of the heart and play a critical role in maintaining cellular function- however, they are also a potent source of free radicals and pro-apoptotic factors. As such, maintaining mitochondrial homeostasis is essential to cell survival. As the dominant source of ATP, continuous quality control is mandatory to ensure their ongoing optimal function. Mitochondrial quality control is accomplished by the dynamic interplay of fusion, fission, autophagy, and mitochondrial biogenesis. This review examines these processes in the heart and considers their role in the context of ischemia-reperfusion injury. Interventions that modulate mitochondrial turnover, including pharmacologic agents, exercise, and caloric restriction are discussed as a means to improve mitochondrial quality control, ameliorate cardiovascular dysfunction, and enhance longevity.
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Cite this article as:
S. Carreira Raquel, Lee Pamela and A. Gottlieb Roberta, Mitochondrial Therapeutics for Cardioprotection, Current Pharmaceutical Design 2011; 17 (20) . https://dx.doi.org/10.2174/138161211796904777
DOI https://dx.doi.org/10.2174/138161211796904777 |
Print ISSN 1381-6128 |
Publisher Name Bentham Science Publisher |
Online ISSN 1873-4286 |
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