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Autophagy in the liver: cell’s cannibalism and beyond

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Abstract

Chronic liver disease and its progression to liver failure are induced by various etiologies including viral infection, alcoholic and nonalcoholic hepatosteatosis. It is anticipated that the prevalence of fatty liver disease will continue to rise due to the growing incidence of obesity and metabolic disorder. Evidence is accumulating to indicate that the onset of fatty liver disease is causatively linked to mitochondrial dysfunction and abnormal lipid accumulation. Current treatment options for this disease are limited. Autophagy is an integral catabolic pathway that maintains cellular homeostasis both selectively and nonselectively. As mitophagy and lipophagy selectively remove dysfunctional mitochondria and excess lipids, respectively, stimulation of autophagy could have therapeutic potential to ameliorate liver function in steatotic patients. This review highlights our up-to-date knowledge on mechanistic roles of autophagy in the pathogenesis of fatty liver disease and its vulnerability to surgical stress, with an emphasis on mitophagy and lipophagy.

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Acknowledgments

This work was supported in part by US National Institutes of Health National Institute of Diabetes and Digestive and Kidney Diseases grant DK079879 and DK090115 (J-S Kim) and National Institute on Aging AG028740 (J-S Kim).

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Flores-Toro, J.A., Go, K.L., Leeuwenburgh, C. et al. Autophagy in the liver: cell’s cannibalism and beyond. Arch. Pharm. Res. 39, 1050–1061 (2016). https://doi.org/10.1007/s12272-016-0807-8

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