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 -
