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Free radical biology for medicine: learning from nonalcoholic fatty liver disease.
Free Radic Biol Med. 2013 Dec; 65:952-968.FR

Abstract

Reactive oxygen species, when released under controlled conditions and limited amounts, contribute to cellular proliferation, senescence, and survival by acting as signaling intermediates. In past decades there has been an epidemic diffusion of nonalcoholic fatty liver disease (NAFLD) that represents the result of the impairment of lipid metabolism, redox imbalance, and insulin resistance in the liver. To date, most studies and reviews have been focused on the molecular mechanisms by which fatty liver progresses to steatohepatitis, but the processes leading toward the development of hepatic steatosis in NAFLD are not fully understood yet. Several nuclear receptors, such as peroxisome proliferator-activated receptors (PPARs) α/γ/δ, PPARγ coactivators 1α and 1β, sterol-regulatory element-binding proteins, AMP-activated protein kinase, liver-X-receptors, and farnesoid-X-receptor, play key roles in the regulation of lipid homeostasis during the pathogenesis of NAFLD. These nuclear receptors may act as redox sensors and may modulate various metabolic pathways in response to specific molecules that act as ligands. It is conceivable that a redox-dependent modulation of lipid metabolism, nuclear receptor-mediated, could cause the development of hepatic steatosis and insulin resistance. Thus, this network may represent a potential therapeutic target for the treatment and prevention of hepatic steatosis and its progression to steatohepatitis. This review summarizes the redox-dependent factors that contribute to metabolism alterations in fatty liver with a focus on the redox control of nuclear receptors in normal liver as well as in NAFLD.

Authors+Show Affiliations

C.U.R.E. Centre for Liver Disease Research and Treatment, Institute of Internal Medicine, Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, Italy. Electronic address: g.serviddio@unifg.it.C.U.R.E. Centre for Liver Disease Research and Treatment, Institute of Internal Medicine, Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, Italy.C.U.R.E. Centre for Liver Disease Research and Treatment, Institute of Internal Medicine, Department of Medical and Surgical Sciences, University of Foggia, 71122 Foggia, Italy.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

23994574

Citation

Serviddio, Gaetano, et al. "Free Radical Biology for Medicine: Learning From Nonalcoholic Fatty Liver Disease." Free Radical Biology & Medicine, vol. 65, 2013, pp. 952-968.
Serviddio G, Bellanti F, Vendemiale G. Free radical biology for medicine: learning from nonalcoholic fatty liver disease. Free Radic Biol Med. 2013;65:952-968.
Serviddio, G., Bellanti, F., & Vendemiale, G. (2013). Free radical biology for medicine: learning from nonalcoholic fatty liver disease. Free Radical Biology & Medicine, 65, 952-968. https://doi.org/10.1016/j.freeradbiomed.2013.08.174
Serviddio G, Bellanti F, Vendemiale G. Free Radical Biology for Medicine: Learning From Nonalcoholic Fatty Liver Disease. Free Radic Biol Med. 2013;65:952-968. PubMed PMID: 23994574.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Free radical biology for medicine: learning from nonalcoholic fatty liver disease. AU - Serviddio,Gaetano, AU - Bellanti,Francesco, AU - Vendemiale,Gianluigi, Y1 - 2013/08/29/ PY - 2013/03/04/received PY - 2013/08/20/revised PY - 2013/08/20/accepted PY - 2013/9/3/entrez PY - 2013/9/3/pubmed PY - 2015/7/15/medline KW - 3-hydroxy-3-methylglutaryl-CoA reductase KW - 4-HNE KW - 4-hydroxynonenal KW - ACC KW - ACOX KW - ALA KW - AMP-activated protein kinase KW - AMPK KW - CAT KW - CPT-1 KW - CREB KW - ER KW - FA KW - FA translocase KW - FAS KW - FAT/CD36 KW - FOX KW - FXR KW - Free radicals KW - G-3-P KW - GPX KW - GRx KW - GSH KW - GST KW - HC KW - HMG-CoAR KW - Hepatic steatosis KW - IRS KW - LXR KW - MAPK KW - MCD KW - NAFLD KW - NASH KW - NFE2L2 KW - NR KW - NRF KW - Nuclear receptors KW - PGC-1α/β KW - PPARα/γ/δ KW - PPARγ coactivators 1α and 1β KW - ROS KW - Redox signaling KW - SCD1 KW - SOD KW - SREBP KW - TAG KW - TCA KW - UCP-2 KW - UPR KW - acetyl-CoA carboxylase KW - acyl-CoA oxidase KW - cAMP-responsive element-binding protein KW - carnitine palmitoyl transferase 1 KW - catalase KW - endoplasmic reticulum KW - farnesoid-X-receptor KW - fatty acid KW - fatty acid synthase KW - forkhead box class KW - glutathione KW - glutathione S-transferase KW - glutathione peroxidase KW - glutathione reductase KW - glycerol 3-phosphate KW - hydroxycholesterol KW - insulin receptor substrate KW - liver-X-receptor KW - malonyl-CoA decarboxylase KW - mitochondrial transcription factor A KW - mitogen-activated protein kinase KW - mtTFA KW - nonalcoholic fatty liver disease KW - nonalcoholic steatohepatitis KW - nuclear factor (erythroid-derived 2)-like 2 KW - nuclear receptor KW - nuclear respiratory factor KW - peroxisome proliferator-activated receptors α/γ/δ KW - reactive oxygen species KW - stearoyl-CoA desaturase-1 KW - sterol-regulatory element-binding protein KW - superoxide dismutase KW - triacylglycerol KW - tricarboxylic acid KW - uncoupling protein 2 KW - unfolded protein response KW - α-lipoic acid SP - 952 EP - 968 JF - Free radical biology & medicine JO - Free Radic Biol Med VL - 65 N2 - Reactive oxygen species, when released under controlled conditions and limited amounts, contribute to cellular proliferation, senescence, and survival by acting as signaling intermediates. In past decades there has been an epidemic diffusion of nonalcoholic fatty liver disease (NAFLD) that represents the result of the impairment of lipid metabolism, redox imbalance, and insulin resistance in the liver. To date, most studies and reviews have been focused on the molecular mechanisms by which fatty liver progresses to steatohepatitis, but the processes leading toward the development of hepatic steatosis in NAFLD are not fully understood yet. Several nuclear receptors, such as peroxisome proliferator-activated receptors (PPARs) α/γ/δ, PPARγ coactivators 1α and 1β, sterol-regulatory element-binding proteins, AMP-activated protein kinase, liver-X-receptors, and farnesoid-X-receptor, play key roles in the regulation of lipid homeostasis during the pathogenesis of NAFLD. These nuclear receptors may act as redox sensors and may modulate various metabolic pathways in response to specific molecules that act as ligands. It is conceivable that a redox-dependent modulation of lipid metabolism, nuclear receptor-mediated, could cause the development of hepatic steatosis and insulin resistance. Thus, this network may represent a potential therapeutic target for the treatment and prevention of hepatic steatosis and its progression to steatohepatitis. This review summarizes the redox-dependent factors that contribute to metabolism alterations in fatty liver with a focus on the redox control of nuclear receptors in normal liver as well as in NAFLD. SN - 1873-4596 UR - https://www.unboundmedicine.com/medline/citation/23994574/Free_radical_biology_for_medicine:_learning_from_nonalcoholic_fatty_liver_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0891-5849(13)00577-7 DB - PRIME DP - Unbound Medicine ER -