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The Complex Interplay Between Metabolism and Apoptosis

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Cell Death

Abstract

Energy balance is essential for cells to function properly and proliferate. Sufficient nutrient quantities are required for energy and the synthesis of building blocks of cellular structures such as lipid membranes, proteins, and nucleic acids. In contrast, nutrient excess can increase ER stress and reactive oxygen species, leading to cellular damage and apoptosis. In this chapter, we detail three important aspects of the interplay between metabolism and apoptosis: the mechanisms by which metabolic imbalances regulate major signaling effectors in apoptosis, how metabolism itself can be controlled by apoptotic proteins, and the major disease states affected when perturbations in metabolism modulate apoptosis.

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Abbreviations

AMPK:

AMP-activated protein kinase

COX:

Cytochrome oxidase

CPT-1:

Carnitine palmitoyltransferase-1

FBPase-2:

Fructose bisphosphatase-2

FFA:

Free fatty acid

Fru-2,6-P2 :

Fructose 2,6-bisphosphate

GAMT:

Guanidinoacetate methyltransferase

HK:

Hexokinase

IMM:

Inner mitochondrial membrane

MOMP:

Mitochondrial outer membrane permeabilization

NAFLD:

Nonalcoholic fatty liver disease

PFK-1:

Phosphofructokinase

PPP:

Pentose phosphate pathway

ROS:

Reactive oxygen species

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Acknowledgements

Thank you to Christopher Freel for help with the creation of the figures and Stephanie Freel and Erika Segear Johnson for critical reading of the chapter. Work on metabolism and apoptosis in the laboratory of SK is supported by NIH GM080333.

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Correspondence to Sally Kornbluth Ph.D. .

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Lindblom, K., Kornbluth, S. (2014). The Complex Interplay Between Metabolism and Apoptosis. In: Wu, H. (eds) Cell Death. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-9302-0_9

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