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AMPK and Metabolic Remodeling in Cardiac Disease

Thomas Pulinilkunnil, Jeevan Nagendran, Jason R.B. Dyck

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Abstract

In all eukaryotes, AMP-activated protein kinase (AMPK) integrates metabolic signals to influence energy balance through the regulation of multiple biochemical pathways. The ability of AMPK to maintain adequate ATP supply at the cellular level plays an important role in the cardiomyocyte since maintaining adequate ATP supply is essential for proper contractile function. In addition, AMPK controls a variety of essential biological processes that also impacts cardiomyocyte function and survival. In this chapter we will discuss the metabolic role of AMPK in modulating glucose and fatty acid transport, oxidation, storage, and the mechanisms by which AMPK influences contractile function and structural remodeling in healthy and diseased hearts. Specifically, we discuss the role that AMPK plays in a variety of conditions such as ischemia/reperfusion injury, cardiac hypertrophy, glycogen storage cardiomyopathy, and Wolff–Parkinson–White syndrome, as well as cardiac dysfunction associated with obesity, insulin resistance, and diabetes. Overall, this chapter summarizes the existing data about the role of AMPK in the heart as well as the role that AMPK plays in the metabolic remodeling that occurs in cardiac disease. Moreover, we pose some pertinent questions, the answers of which may help provide additional insight into the metabolic role of AMPK in diseased hearts. This information may eventually help in the development of therapeutic approaches that target AMPK or AMPK-regulated pathways to improve function of metabolically remodeled diseased hearts. These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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What this paper is about

In all eukaryotes, AMP-activated protein kinase (AMPK) integrates metabolic signals to influence energy balance through the regulation of multiple biochemical pathways. The ability of AMPK to maintain adequate ATP supply at the cellular level plays an important role in the cardiomyocyte since maintaining adequate ATP supply is essential for proper contractile function. In addition, AMPK controls a variety of essential biological processes that also impacts cardiomyocyte function and survival. In this chapter we will discuss the metabolic role of AMPK in modulating glucose and fatty acid transport, oxidation, storage, and the mechanisms by which AMPK influences contractile function and structural remodeling in healthy and diseased hearts. Specifically, we discuss the role that AMPK plays in a variety of conditions such as ischemia/reperfusion injury, cardiac hypertrophy, glycogen storage cardiomyopathy, and Wolff–Parkinson–White syndrome, as well as cardiac dysfunction associated with obesity, insulin resistance, and diabetes. Overall, this chapter summarizes the existing data about the role of AMPK in the heart as well as the role that AMPK plays in the metabolic remodeling that occurs in cardiac disease. Moreover, we pose some pertinent questions, the answers of which may help provide additional insight into the metabolic role of AMPK in diseased hearts. This information may eventually help in the development of therapeutic approaches that target AMPK or AMPK-regulated pathways to improve function of metabolically remodeled diseased hearts. These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Available abstract

In all eukaryotes, AMP-activated protein kinase (AMPK) integrates metabolic signals to influence energy balance through the regulation of multiple biochemical pathways. The ability of AMPK to maintain adequate ATP supply at the cellular level plays an important role in the cardiomyocyte since maintaining adequate ATP supply is essential for proper contractile function. In addition, AMPK controls a variety of essential biological processes that also impacts cardiomyocyte function and survival. In this chapter we will discuss the metabolic role of AMPK in modulating glucose and fatty acid transport, oxidation, storage, and the mechanisms by which AMPK influences contractile function and structural remodeling in healthy and diseased hearts. Specifically, we discuss the role that AMPK plays in a variety of conditions such as ischemia/reperfusion injury, cardiac hypertrophy, glycogen storage cardiomyopathy, and Wolff–Parkinson–White syndrome, as well as cardiac dysfunction associated with obesity, insulin resistance, and diabetes. Overall, this chapter summarizes the existing data about the role of AMPK in the heart as well as the role that AMPK plays in the metabolic remodeling that occurs in cardiac disease. Moreover, we pose some pertinent questions, the answers of which may help provide additional insight into the metabolic role of AMPK in diseased hearts. This information may eventually help in the development of therapeutic approaches that target AMPK or AMPK-regulated pathways to improve function of metabolically remodeled diseased hearts. These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Key concepts: AMPK, Protein kinase A, AMP-activated protein kinase, Beta oxidation, Diabetic cardiomyopathy, Medicine, Cardiomyopathy, Biology

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