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Article ; Online: Corrigendum to "Acid ceramidase improves mitochondrial function and oxidative stress in Niemann-Pick type C disease by repressing STARD1 expression and mitochondrial cholesterol accumulation" [Redox Biol. 2021 45 102052].

Torres, S / Solsona-Vilarrasa, E / Nuñez, S / Matías, N / Insausti-Urkia, N / Castro, F / Casasempere, M / Fabriás, G / Casas, J / Enrich, C / Fernández-Checa, J C / Garcia-Ruiz, C

Redox biology

2022 Volume 50, Page(s) 102231

Language	English
Publishing date	2022-01-10
Publishing country	Netherlands
Document type	Published Erratum
ZDB-ID	2701011-9
ISSN	2213-2317 ; 2213-2317
ISSN (online)	2213-2317
ISSN	2213-2317
DOI	10.1016/j.redox.2022.102231
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Article ; Online: JNK interaction with Sab mediates ER stress induced inhibition of mitochondrial respiration and cell death.

Win, S / Than, T A / Fernandez-Checa, J C / Kaplowitz, N

Cell death & disease

2014 Volume 5, Page(s) e989

Abstract: Our aim was to better understand the mechanism and importance of sustained c-Jun N-terminal kinase (JNK) activation in endoplasmic reticulum (ER) stress and effects of ER stress on mitochondria by determining the role of mitochondrial JNK binding protein, ...

Abstract	Our aim was to better understand the mechanism and importance of sustained c-Jun N-terminal kinase (JNK) activation in endoplasmic reticulum (ER) stress and effects of ER stress on mitochondria by determining the role of mitochondrial JNK binding protein, Sab. Tunicamycin or brefeldin A induced a rapid and marked decline in basal mitochondrial respiration and reserve-capacity followed by delayed mitochondrial-mediated apoptosis. Knockdown of mitochondrial Sab prevented ER stress-induced sustained JNK activation, impaired respiration, and apoptosis, but did not alter the magnitude or time course of activation of ER stress pathways. P-JNK plus adenosine 5'-triphosphate (ATP) added to isolated liver mitochondria promoted superoxide production, which was amplified by addition of calcium and inhibited by a blocking peptide corresponding to the JNK binding site on Sab (KIM1). This peptide also blocked tunicamycin-induced inhibition of cellular respiration. In conclusion, ER stress triggers an interaction of JNK with mitochondrial Sab, which leads to impaired respiration and increased mitochondrial reactive oxygen species, sustaining JNK activation culminating in apoptosis.
MeSH term(s)	Adenosine Triphosphate/metabolism ; Animals ; Apoptosis ; Cell Respiration ; Cells, Cultured ; Down-Regulation ; Endoplasmic Reticulum Stress ; Hepatocytes/cytology ; Hepatocytes/enzymology ; Hepatocytes/metabolism ; Humans ; JNK Mitogen-Activated Protein Kinases/genetics ; JNK Mitogen-Activated Protein Kinases/metabolism ; Male ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Inbred C57BL ; Mitochondria/genetics ; Mitochondria/metabolism ; Mitochondrial Proteins/genetics ; Mitochondrial Proteins/metabolism ; Protein Binding ; Reactive Oxygen Species/metabolism
Chemical Substances	Membrane Proteins ; Mitochondrial Proteins ; Reactive Oxygen Species ; Sab protein, mouse ; Adenosine Triphosphate (8L70Q75FXE) ; JNK Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2014-01-09
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/cddis.2013.522
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Article ; Online: Roadmap to DILI research in Europe. A proposal from COST action ProEuroDILINet.

Pharmacological research

2023 Volume 200, Page(s) 107046

Abstract: In the current article the aims for a constructive way forward in Drug-Induced Liver Injury (DILI) are to highlight the most important priorities in research and clinical science, therefore supporting a more informed, focused, and better funded future ... ...

Abstract	In the current article the aims for a constructive way forward in Drug-Induced Liver Injury (DILI) are to highlight the most important priorities in research and clinical science, therefore supporting a more informed, focused, and better funded future for European DILI research. This Roadmap aims to identify key challenges, define a shared vision across all stakeholders for the opportunities to overcome these challenges and propose a high-quality research program to achieve progress on the prediction, prevention, diagnosis and management of this condition and impact on healthcare practice in the field of DILI. This will involve 1. Creation of a database encompassing optimised case report form for prospectively identified DILI cases with well-characterised controls with competing diagnoses, biological samples, and imaging data; 2. Establishing of preclinical models to improve the assessment and prediction of hepatotoxicity in humans to guide future drug safety testing; 3. Emphasis on implementation science and 4. Enhanced collaboration between drug-developers, clinicians and regulatory scientists. This proposed operational framework will advance DILI research and may bring together basic, applied, translational and clinical research in DILI.
MeSH term(s)	Humans ; Chemical and Drug Induced Liver Injury ; Europe ; Drug-Related Side Effects and Adverse Reactions ; Forecasting ; Databases, Factual
Language	English
Publishing date	2023-12-28
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	1003347-6
ISSN	1096-1186 ; 0031-6989 ; 1043-6618
ISSN (online)	1096-1186
ISSN	0031-6989 ; 1043-6618
DOI	10.1016/j.phrs.2023.107046
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Zs.A 721: Show issues

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Article ; Online: Mitochondrial dysfunction in non-alcoholic fatty liver disease and insulin resistance: cause or consequence?

García-Ruiz, C / Baulies, A / Mari, M / García-Rovés, P M / Fernandez-Checa, J C

Free radical research

2013 Volume 47, Issue 11, Page(s) 854–868

Abstract: Non-alcoholic fatty liver disease (NAFLD) is considered the hepatic manifestation of the metabolic syndrome and refers to a spectrum of disorders ranging from steatosis to steatohepatitis, a disease stage characterized by inflammation, fibrosis, cell ... ...

Abstract	Non-alcoholic fatty liver disease (NAFLD) is considered the hepatic manifestation of the metabolic syndrome and refers to a spectrum of disorders ranging from steatosis to steatohepatitis, a disease stage characterized by inflammation, fibrosis, cell death and insulin resistance (IR). Due to its association with obesity and IR the impact of NAFLD is growing worldwide. Consistent with the role of mitochondria in fatty acid (FA) metabolism, impaired mitochondrial function is thought to contribute to NAFLD and IR. Indeed, mitochondrial dysfunction and impaired mitochondrial respiratory chain have been described in patients with non-alcoholic steatohepatitis and skeletal muscle of obese patients. However, recent data have provided evidence that pharmacological and genetic models of mitochondrial impairment with reduced electron transport stimulate insulin sensitivity and protect against diet-induced obesity, hepatosteatosis and IR. These beneficial metabolic effects of impaired mitochondrial oxidative phosphorylation may be related not only to the reduction of reactive oxygen species production that regulate insulin signaling but also to decreased mitochondrial FA overload that generate specific metabolites derived from incomplete FA oxidation (FAO) in the TCA cycle. In line with the Randle cycle, reduced mitochondrial FAO rates may alleviate the repression on glucose metabolism in obesity. In addition, the redox paradox in insulin signaling and the delicate mitochondrial antioxidant balance in steatohepatitis add another level of complexity to the role of mitochondria in NAFLD and IR. Thus, better understanding the role of mitochondria in FA metabolism and glucose homeostasis may provide novel strategies for the treatment of NAFLD and IR.
MeSH term(s)	Animals ; Fatty Liver/metabolism ; Humans ; Insulin Resistance/physiology ; Lipid Metabolism ; Metabolic Syndrome/metabolism ; Mitochondria/metabolism ; Non-alcoholic Fatty Liver Disease
Language	English
Publishing date	2013-11
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1194130-3
ISSN	1029-2470 ; 1071-5762
ISSN (online)	1029-2470
ISSN	1071-5762
DOI	10.3109/10715762.2013.830717
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Zs.A 2236: Show issues

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Article: Alcoholic liver disease.

Fernández-Checa, J C

Methods and findings in experimental and clinical pharmacology

1996 Volume 18 Suppl B, Page(s) 27–31

MeSH term(s)	Alcoholic Intoxication/complications ; Animals ; Ethanol/adverse effects ; Humans ; Liver/metabolism ; Liver/pathology ; Liver Diseases, Alcoholic/blood ; Liver Diseases, Alcoholic/etiology ; Microsomes, Liver/enzymology ; Tumor Necrosis Factor-alpha/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Tumor Necrosis Factor-alpha ; Ethanol (3K9958V90M)
Language	English
Publishing date	1996
Publishing country	Spain
Document type	Journal Article
ZDB-ID	446847-8
ISSN	2013-0155 ; 0379-0355
ISSN (online)	2013-0155
ISSN	0379-0355
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Zs.A 1525: Show issues

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Article ; Online: Oxidative stress and altered mitochondrial function in neurodegenerative diseases: lessons from mouse models.

Fernández-Checa, J C / Fernández, A / Morales, A / Marí, M / García-Ruiz, C / Colell, A

CNS & neurological disorders drug targets

2010 Volume 9, Issue 4, Page(s) 439–454

Abstract: Oxidative stress has been consistently linked to ageing-related neurodegenerative diseases leading to the generation of lipid peroxides, carbonyl proteins and oxidative DNA damage in tissue samples from affected brains. Studies from mouse models that ... ...

Abstract	Oxidative stress has been consistently linked to ageing-related neurodegenerative diseases leading to the generation of lipid peroxides, carbonyl proteins and oxidative DNA damage in tissue samples from affected brains. Studies from mouse models that express disease-specific mutant proteins associated to the major neurodegenerative processes have underscored a critical role of mitochondria in the pathogenesis of these diseases. There is strong evidence that mitochondrial dysfunction is an early event in neurodegeneration. Mitochondria are the main cellular source of reactive oxygen species and key regulators of cell death. Moreover, mitochondria are highly dynamic organelles that divide, fuse and move along axons and dendrites to supply cellular energetic demands; therefore, impairment of any of these processes would directly impact on neuronal viability. Most of the disease-specific pathogenic mutant proteins have been shown to target mitochondria, promoting oxidative stress and the mitochondrial apoptotic pathway. In addition, disease-specific mutant proteins may also impair mitochondrial dynamics and recycling of damaged mitochondria via autophagy. Collectively, these data suggest that ROS-mediated defective mitochondria may accumulate during and contribute to disease progression. Strategies aimed to improve mitochondrial function or ROS scavenging may thus be of potential clinical relevance.
MeSH term(s)	Animals ; Brain/metabolism ; Brain/physiopathology ; Disease Models, Animal ; Humans ; Mice ; Mitochondria/genetics ; Mitochondria/physiology ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/physiopathology ; Oxidative Stress/genetics ; Oxidative Stress/physiology ; Reactive Oxygen Species/metabolism ; Superoxide Dismutase/genetics ; Superoxide Dismutase/metabolism ; Superoxide Dismutase/physiology
Chemical Substances	Reactive Oxygen Species ; Superoxide Dismutase (EC 1.15.1.1)
Language	English
Publishing date	2010-06-11
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2228394-8
ISSN	1996-3181 ; 1871-5273
ISSN (online)	1996-3181
ISSN	1871-5273
DOI	10.2174/187152710791556113
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Zs.A 5892: Show issues

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Article: Brain mitochondrial alterations after chronic alcohol consumption.

Almansa, I / Fernández, A / García-Ruiz, C / Muriach, M / Barcia, J M / Miranda, M / Fernández-Checa, J C / Romero, F J

Journal of physiology and biochemistry

2010 Volume 65, Issue 3, Page(s) 305–312

Abstract: The aim of this study was to demonstrate the existence of alterations in glutathione and cholesterol homeostasis in brain mitochondria from alcoholic rats. Glutathione concentration decreased, whereas oxidized glutathione and cholesterol contents ... ...

Abstract	The aim of this study was to demonstrate the existence of alterations in glutathione and cholesterol homeostasis in brain mitochondria from alcoholic rats. Glutathione concentration decreased, whereas oxidized glutathione and cholesterol contents increased in these organelles, suggesting the ethanol-induced generation of reactive oxygen species, and the impairment of mitochondrial uptake of glutathione, possibly due to the increase in cholesterol deposition. The release of apoptogenic proteins was increased after stimulating mitochondria from the brain of alcoholic rats with atractyloside. As a conclusion, chronic alcohol consumption might sensitize brain mitochondria to apoptotic stimuli, and promote the subsequent release of apoptotic proteins.
MeSH term(s)	Alcoholism/metabolism ; Animals ; Apoptosis Regulatory Proteins ; Brain/metabolism ; Brain/pathology ; Brain/ultrastructure ; Carrier Proteins/metabolism ; Cholesterol/metabolism ; Cytochromes c/metabolism ; Ethanol/pharmacology ; Glutathione/metabolism ; Glutathione Disulfide/metabolism ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mitochondrial Proteins/metabolism ; Rats ; Rats, Sprague-Dawley
Chemical Substances	Apoptosis Regulatory Proteins ; Carrier Proteins ; DIABLO protein, rat ; Mitochondrial Proteins ; Ethanol (3K9958V90M) ; Cytochromes c (9007-43-6) ; Cholesterol (97C5T2UQ7J) ; Glutathione (GAN16C9B8O) ; Glutathione Disulfide (ULW86O013H)
Language	English
Publishing date	2010-01-30
Publishing country	Spain
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1325104-1
ISSN	1138-7548 ; 0034-9402
ISSN	1138-7548 ; 0034-9402
DOI	10.1007/BF03180583
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Zs.B 198: Show issues

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Article: Oxidative stress and alcoholic liver disease.

Fernández-Checa, J C / Kaplowitz, N / Colell, A / García-Ruiz, C

Alcohol health and research world

2004 Volume 21, Issue 4, Page(s) 321–324

Abstract: Toxic substances generated during the metabolism of alcohol in the liver may contribute to the development of alcoholic liver disease. These substances include highly reactive molecules that can destroy vital cell components through a process called ... ...

Abstract	Toxic substances generated during the metabolism of alcohol in the liver may contribute to the development of alcoholic liver disease. These substances include highly reactive molecules that can destroy vital cell components through a process called oxidation. Cells are protected against oxidation by the action of certain enzymes, vitamins, and other substances, known collectively as antioxidants. An imbalance between oxidants and antioxidants can lead to oxidative stress, characterized by escalating cell damage. Evidence suggests that the major energy-generating structures within cells (i.e., mitochondria) may be especially sensitive to oxidative stress, resulting in diminished energy production. Medications that reduce oxidative stress in mitochondria may ameliorate liver disease.
MeSH term(s)	Animals ; Humans ; Liver Diseases, Alcoholic/metabolism ; Liver Diseases, Alcoholic/pathology ; Oxidative Stress/physiology
Language	English
Publishing date	2004-10-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S. ; Review
ZDB-ID	427760-0
ISSN	0090-838X
ISSN	0090-838X
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Zs.B 2180: Show issues

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Article: Sensitivity of the 2-oxoglutarate carrier to alcohol intake contributes to mitochondrial glutathione depletion.

Coll, Olga / Colell, Anna / García-Ruiz, Carmen / Kaplowitz, Neil / Fernández-Checa, J C

Hepatology (Baltimore, Md.)

2003 Volume 38, Issue 3, Page(s) 692–702

Abstract: The mitochondrial pool of reduced glutathione (mGSH) is known to play a protective role against liver injury and cytokine-mediated cell death. However, the identification of the mitochondrial carriers involved in its transport in hepatocellular ... ...

Abstract	The mitochondrial pool of reduced glutathione (mGSH) is known to play a protective role against liver injury and cytokine-mediated cell death. However, the identification of the mitochondrial carriers involved in its transport in hepatocellular mitochondria remains unestablished. In this study, we show that the functional expression of the 2-oxoglutarate carrier from HepG2 cells in mitochondria from Xenopus laevis oocytes conferred a reduced glutathione (GSH) transport activity that was inhibited by phenylsuccinate, a specific inhibitor of the carrier. In addition, the mitochondrial transport of GSH and 2-oxoglutarate in isolated mitochondria from rat liver exhibited mutual competition and sensitivity to glutamate and phenylsuccinate. Interestingly, the kinetics of 2-oxoglutarate transport in rat liver mitochondria displayed a single Michaelis-Menten component with a Michaelis constant of 3.1 +/- 0.3 mmol/L and maximum velocity of 1.9 +/- 0.1 nmol/mg protein/25 seconds. Furthermore, the initial rate of 2-oxoglutarate was reduced in mitochondria from alcohol-fed rat livers, an effect that was not accompanied by an alcohol-induced decrease in the 2-oxoglutarate messenger RNA levels but rather by changes in mitochondrial membrane dynamics induced by alcohol. The fluidization of mitochondria by the fluidizing agent 2-(2-methoxyethoxy)ethyl 8-(cis-2-n-octylcyclopropyl) (A(2)C) restored the initial transport rate of both GSH and 2-oxoglutarate. Finally, these changes were reproduced in normal liver mitochondria enriched in cholesterol where the fluidization of cholesterol-enriched mitochondria with A(2)C restored the order membrane parameter and the mitochondrial 2-oxoglutarate uptake. In conclusion, these findings provide unequivocal evidence for 2-oxoglutarate as a GSH carrier and its sensitivity to membrane dynamics perturbation contributes in part to the alcohol-induced mGSH depletion.
MeSH term(s)	Alcohol Drinking/metabolism ; Animals ; Biological Transport/drug effects ; Carrier Proteins/metabolism ; Cholesterol/pharmacology ; Glutathione/deficiency ; Glutathione/metabolism ; Humans ; Male ; Membrane Fluidity ; Membrane Transport Proteins ; Mitochondria, Liver/metabolism ; Oocytes ; Rats ; Rats, Sprague-Dawley ; Xenopus laevis
Chemical Substances	Carrier Proteins ; Membrane Transport Proteins ; oxoglutarate translocator ; Cholesterol (97C5T2UQ7J) ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2003-09
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	604603-4
ISSN	1527-3350 ; 0270-9139
ISSN (online)	1527-3350
ISSN	0270-9139
DOI	10.1053/jhep.2003.50351
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Zs.A 1660: Show issues

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Article: Pharmacological inhibition or small interfering RNA targeting acid ceramidase sensitizes hepatoma cells to chemotherapy and reduces tumor growth in vivo.

Morales, A / París, R / Villanueva, A / Llacuna, L / García-Ruiz, C / Fernández-Checa, J C

Oncogene

2007 Volume 26, Issue 6, Page(s) 905–916

Abstract: Ceramidases (CDases) play a key role in cancer therapy through enhanced conversion of ceramide into sphingosine 1-phosphate (S1P), but their involvement in hepatocarcinogenesis is unknown. Here, we report that daunorubicin (DNR) activated acid CDase post- ...

Abstract	Ceramidases (CDases) play a key role in cancer therapy through enhanced conversion of ceramide into sphingosine 1-phosphate (S1P), but their involvement in hepatocarcinogenesis is unknown. Here, we report that daunorubicin (DNR) activated acid CDase post-transcriptionally in established human (HepG2 cells) or mouse (Hepa1c1c7) hepatoma cell lines as well as in primary cells from murine liver tumors, but not in cultured mouse hepatocytes. Acid CDase silencing by small interfering RNA (siRNA) or pharmacological inhibition with N-oleoylethanolamine (NOE) enhanced the ceramide to S1P balance compared to DNR alone, sensitizing hepatoma cells (HepG2, Hep-3B, SK-Hep and Hepa1c1c7) to DNR-induced cell death. DNR plus NOE or acid CDase siRNA-induced cell death was preceded by ultrastructural changes in mitochondria, stimulation of reactive oxygen species generation, release of Smac/DIABLO and cytochrome c and caspase-3 activation. In addition, in vivo siRNA treatment targeting acid CDase reduced tumor growth in liver tumor xenografts of HepG2 cells and enhanced DNR therapy. Thus, acid CDase promotes hepatocarcinogenesis and its antagonism may be a promising strategy in the treatment of liver cancer.
MeSH term(s)	Animals ; Carcinoma, Hepatocellular/drug therapy ; Carcinoma, Hepatocellular/enzymology ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/pathology ; Caspase 3/metabolism ; Cell Proliferation/drug effects ; Daunorubicin/pharmacology ; Daunorubicin/toxicity ; Drug Therapy ; Endocannabinoids ; Ethanolamines/pharmacology ; Galactosylgalactosylglucosylceramidase/antagonists & inhibitors ; Galactosylgalactosylglucosylceramidase/genetics ; Galactosylgalactosylglucosylceramidase/metabolism ; Humans ; Lysophospholipids/metabolism ; Mice ; Microscopy, Electron, Transmission ; Mitochondria/drug effects ; Mitochondria/enzymology ; Oleic Acids ; Protease Inhibitors/pharmacology ; RNA, Messenger/genetics ; RNA, Small Interfering/genetics ; Sphingosine/analogs & derivatives ; Sphingosine/metabolism ; Tumor Cells, Cultured ; Xenograft Model Antitumor Assays
Chemical Substances	Endocannabinoids ; Ethanolamines ; Lysophospholipids ; Oleic Acids ; Protease Inhibitors ; RNA, Messenger ; RNA, Small Interfering ; N-oleoylethanolamine (111-58-0) ; sphingosine 1-phosphate (26993-30-6) ; Galactosylgalactosylglucosylceramidase (EC 3.2.1.47) ; Caspase 3 (EC 3.4.22.-) ; Sphingosine (NGZ37HRE42) ; Daunorubicin (ZS7284E0ZP)
Language	English
Publishing date	2007-02-08
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/sj.onc.1209834
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