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  1. Book ; Online: Autophagy and Related Transcription Factors in Liver and Gut Diseases

    Eid, Nabil / Thomes, Paul / Menon, Manoj B. / Zeng, Tao / Raimundo, Nuno / Fernandez-Checa, Jose C. / Wang, Lin

    2020  

    Keywords Science: general issues ; Pharmacology ; Autophagy ; Lipophagy ; Liver ; Gut ; Diseases
    Size 1 electronic resource (109 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021230328
    ISBN 9782889635467 ; 2889635465
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: HILPDA, a new player in NASH-driven HCC, links hypoxia signaling with ceramide synthesis.

    Fernandez-Checa, Jose C / Torres, Sandra / Garcia-Ruiz, Carmen

    Journal of hepatology

    2023  Volume 79, Issue 2, Page(s) 269–272

    MeSH term(s) Humans ; Carcinoma, Hepatocellular/etiology ; Liver Neoplasms/etiology ; Non-alcoholic Fatty Liver Disease/complications ; Hypoxia ; Ceramides
    Chemical Substances Ceramides
    Language English
    Publishing date 2023-05-17
    Publishing country Netherlands
    Document type Editorial ; Comment
    ZDB-ID 605953-3
    ISSN 1600-0641 ; 0168-8278
    ISSN (online) 1600-0641
    ISSN 0168-8278
    DOI 10.1016/j.jhep.2023.05.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2027: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: C-Reactive Protein, a Promising Approach for Acetaminophen Hepatotoxicity.

    Garcia-Ruiz, Carmen / Fernandez-Checa, Jose C

    Cellular and molecular gastroenterology and hepatology

    2021  Volume 13, Issue 1, Page(s) 341–342

    MeSH term(s) Acetaminophen ; C-Reactive Protein ; Chemical and Drug Induced Liver Injury ; Humans
    Chemical Substances Acetaminophen (362O9ITL9D) ; C-Reactive Protein (9007-41-4)
    Language English
    Publishing date 2021-10-31
    Publishing country United States
    Document type Editorial ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2819778-1
    ISSN 2352-345X ; 2352-345X
    ISSN (online) 2352-345X
    ISSN 2352-345X
    DOI 10.1016/j.jcmgh.2021.10.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Mitochondria and the NLRP3 Inflammasome in Alcoholic and Nonalcoholic Steatohepatitis.

    Torres, Sandra / Segalés, Paula / García-Ruiz, Carmen / Fernández-Checa, José C

    Cells

    2022  Volume 11, Issue 9

    Abstract: Alcoholic (ASH) and nonalcoholic steatohepatitis (NASH) are advanced stages of fatty liver disease and two of the most prevalent forms of chronic liver disease. ASH and NASH are associated with significant risk of further progression to cirrhosis and ... ...

    Abstract Alcoholic (ASH) and nonalcoholic steatohepatitis (NASH) are advanced stages of fatty liver disease and two of the most prevalent forms of chronic liver disease. ASH and NASH are associated with significant risk of further progression to cirrhosis and hepatocellular carcinoma (HCC), the most common type of liver cancer, and a major cause of cancer-related mortality. Despite extensive research and progress in the last decades to elucidate the mechanisms of the development of ASH and NASH, the pathogenesis of both diseases is still poorly understood. Mitochondrial damage and activation of inflammasome complexes have a role in inducing and sustaining liver damage. Mitochondrial dysfunction produces inflammatory factors that activate the inflammasome complexes. NLRP3 inflammasome (nucleotide-binding oligomerization domain-like receptor protein 3) is a multiprotein complex that activates caspase 1 and the release of pro-inflammatory cytokines, including interleukin-1β (IL-1β) and interleukin-18 (IL-18), and contributes to inflammatory pyroptotic cell death. The present review, which is part of the issue "Mitochondria in Liver Pathobiology", provides an overview of the role of mitochondrial dysfunction and NLRP3 activation in ASH and NASH.
    MeSH term(s) Carcinoma, Hepatocellular ; Humans ; Inflammasomes/metabolism ; Liver Neoplasms ; Mitochondria/metabolism ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Non-alcoholic Fatty Liver Disease/metabolism
    Chemical Substances Inflammasomes ; NLR Family, Pyrin Domain-Containing 3 Protein
    Language English
    Publishing date 2022-04-27
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells11091475
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Mitochondrial cholesterol: Metabolism and impact on redox biology and disease.

    Goicoechea, Leire / Conde de la Rosa, Laura / Torres, Sandra / García-Ruiz, Carmen / Fernández-Checa, José C

    Redox biology

    2023  Volume 61, Page(s) 102643

    Abstract: Cholesterol is a crucial component of membrane bilayers by regulating their structural and functional properties. Cholesterol traffics to different cellular compartments including mitochondria, whose cholesterol content is low compared to other cell ... ...

    Abstract Cholesterol is a crucial component of membrane bilayers by regulating their structural and functional properties. Cholesterol traffics to different cellular compartments including mitochondria, whose cholesterol content is low compared to other cell membranes. Despite the limited availability of cholesterol in the inner mitochondrial membrane (IMM), the metabolism of cholesterol in the IMM plays important physiological roles, acting as the precursor for the synthesis of steroid hormones and neurosteroids in steroidogenic tissues and specific neurons, respectively, or the synthesis of bile acids through an alternative pathway in the liver. Accumulation of cholesterol in mitochondria above physiological levels has a negative impact on mitochondrial function through several mechanisms, including the limitation of crucial antioxidant defenses, such as the glutathione redox cycle, increased generation of reactive oxygen species and consequent oxidative modification of cardiolipin, and defective assembly of respiratory supercomplexes. These adverse consequences of increased mitochondrial cholesterol trafficking trigger the onset of oxidative stress and cell death, and, ultimately, contribute to the development of diverse diseases, including metabolic liver diseases (i.e. fatty liver disease and liver cancer), as well as lysosomal disorders (i.e. Niemann-Pick type C disease) and neurodegenerative diseases (i.e. Alzheimer's disease). In this review, we summarize the metabolism and regulation of mitochondrial cholesterol and its potential impact on liver and neurodegenerative diseases.
    MeSH term(s) Humans ; Mitochondria/metabolism ; Oxidation-Reduction ; Cholesterol/metabolism ; Neurodegenerative Diseases/metabolism ; Biology
    Chemical Substances Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 2023-02-24
    Publishing country Netherlands
    Document type Review ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2023.102643
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: S-Adenosyl-l-methionine restores brain mitochondrial membrane fluidity and GSH content improving Niemann-Pick type C disease.

    Goicoechea, Leire / Torres, Sandra / Fàbrega, Laura / Barrios, Mónica / Núñez, Susana / Casas, Josefina / Fabrias, Gemma / García-Ruiz, Carmen / Fernández-Checa, José C

    Redox biology

    2024  Volume 72, Page(s) 103150

    Abstract: Niemann-Pick type C (NPC) disease is a lysosomal storage disorder characterized by impaired motor coordination due to neurological defects and cerebellar dysfunction caused by the accumulation of cholesterol in endolysosomes. Besides the increase in ... ...

    Abstract Niemann-Pick type C (NPC) disease is a lysosomal storage disorder characterized by impaired motor coordination due to neurological defects and cerebellar dysfunction caused by the accumulation of cholesterol in endolysosomes. Besides the increase in lysosomal cholesterol, mitochondria are also enriched in cholesterol, which leads to decreased membrane fluidity, impaired mitochondrial function and loss of GSH, and has been shown to contribute to the progression of NPC disease. S-Adenosyl-l-methionine (SAM) regulates membrane physical properties through the generation of phosphatidylcholine (PC) from phosphatidylethanolamine (PE) methylation and functions as a GSH precursor by providing cysteine in the transsulfuration pathway. However, the role of SAM in NPC disease has not been investigated. Here we report that Npc1
    MeSH term(s) Animals ; Mice ; Membrane Fluidity ; S-Adenosylmethionine/metabolism ; Mitochondrial Membranes/metabolism ; Niemann-Pick Disease, Type C/metabolism ; Niemann-Pick Disease, Type C/drug therapy ; Niemann-Pick Disease, Type C/genetics ; Glutathione/metabolism ; Brain/metabolism ; Mitochondria/metabolism ; Niemann-Pick C1 Protein ; Disease Models, Animal ; Mice, Knockout ; Phosphatidylcholines/metabolism
    Chemical Substances S-Adenosylmethionine (7LP2MPO46S) ; Glutathione (GAN16C9B8O) ; Niemann-Pick C1 Protein ; Npc1 protein, mouse ; Phosphatidylcholines
    Language English
    Publishing date 2024-04-03
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2024.103150
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Mitochondrial Oxidative Stress and Antioxidants Balance in Fatty Liver Disease.

    García-Ruiz, Carmen / Fernández-Checa, José C

    Hepatology communications

    2018  Volume 2, Issue 12, Page(s) 1425–1439

    Abstract: Fatty liver disease is one of the most prevalent forms of chronic liver disease that encompasses both alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD). Alcoholic steatohepatitis (ASH) and nonalcoholic steatohepatitis (NASH) are ... ...

    Abstract Fatty liver disease is one of the most prevalent forms of chronic liver disease that encompasses both alcoholic liver disease (ALD) and nonalcoholic fatty liver disease (NAFLD). Alcoholic steatohepatitis (ASH) and nonalcoholic steatohepatitis (NASH) are intermediate stages of ALD and NAFLD, which can progress to more advanced forms, including cirrhosis and hepatocellular carcinoma. Oxidative stress and particularly alterations in mitochondrial function are thought to play a significant role in both ASH and NASH and recognized to contribute to the generation of reactive oxygen species (ROS), as documented in experimental models. Despite the evidence of ROS generation, the therapeutic efficacy of treatment with antioxidants in patients with fatty liver disease has yielded poor results. Although oxidative stress is considered to be the disequilibrium between ROS and antioxidants, there is evidence that a subtle balance among antioxidants, particularly in mitochondria, is necessary to avoid the generation of ROS and hence oxidative stress.
    Language English
    Publishing date 2018-10-30
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2471-254X
    ISSN (online) 2471-254X
    DOI 10.1002/hep4.1271
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Editorial: lipids in cancer cell biology and therapy.

    Fernandez-Checa, Jose C

    Anti-cancer agents in medicinal chemistry

    2012  Volume 12, Issue 4, Page(s) 283–284

    MeSH term(s) Apoptosis ; Cholesterol/metabolism ; Humans ; Neoplasms/metabolism ; Neoplasms/therapy ; Sphingolipids/metabolism
    Chemical Substances Sphingolipids ; Cholesterol (97C5T2UQ7J)
    Language English
    Publishing date 2012-02-23
    Publishing country Netherlands
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 2217610-X
    ISSN 1875-5992 ; 1871-5206
    ISSN (online) 1875-5992
    ISSN 1871-5206
    DOI 10.2174/187152012800228625
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5583: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  9. Article: Mitochondrial Cholesterol in Alzheimer's Disease and Niemann-Pick Type C Disease.

    Torres, Sandra / García-Ruiz, Carmen M / Fernandez-Checa, Jose C

    Frontiers in neurology

    2019  Volume 10, Page(s) 1168

    Abstract: Mitochondrial dysfunction has been recognized as a key player in neurodegenerative diseases, including Alzheimer's disease (AD) and Niemann-Pick type C (NPC) disease. While the pathogenesis of both diseases is different, disruption of intracellular ... ...

    Abstract Mitochondrial dysfunction has been recognized as a key player in neurodegenerative diseases, including Alzheimer's disease (AD) and Niemann-Pick type C (NPC) disease. While the pathogenesis of both diseases is different, disruption of intracellular cholesterol trafficking has emerged as a common feature of both AD and NPC disease. Nutritional or genetic mitochondrial cholesterol accumulation sensitizes neurons to Aβ-mediated neurotoxicity
    Language English
    Publishing date 2019-11-07
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2564214-5
    ISSN 1664-2295
    ISSN 1664-2295
    DOI 10.3389/fneur.2019.01168
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Dietary and genetic disruption of hepatic methionine metabolism induce acid sphingomyelinase to promote steatohepatitis.

    Alarcón-Vila, Cristina / Insausti-Urkia, Naroa / Torres, Sandra / Segalés-Rovira, Paula / Conde de la Rosa, Laura / Nuñez, Susana / Fucho, Raquel / Fernández-Checa, Jose C / García-Ruiz, Carmen

    Redox biology

    2023  Volume 59, Page(s) 102596

    Abstract: Alcoholic (ASH) and nonalcoholic. (NASH).steatohepatitis are advanced.stages.of.fatty.liver.disease.Methionine adenosyltransferase 1A (MAT1A) plays a key role in hepatic methionine metabolism and germline Mat1a deletion in mice promotes NASH. Acid ... ...

    Abstract Alcoholic (ASH) and nonalcoholic. (NASH).steatohepatitis are advanced.stages.of.fatty.liver.disease.Methionine adenosyltransferase 1A (MAT1A) plays a key role in hepatic methionine metabolism and germline Mat1a deletion in mice promotes NASH. Acid sphingomyelinase (ASMase) triggers hepatocellular apoptosis and liver fibrosis and has been shown to downregulate MAT1A expression in the context of fulminant liver failure. Given the role of ASMase in steatohepatitis development, we investigated the status of ASMase in Mat1a
    MeSH term(s) Animals ; Mice ; Amitriptyline/pharmacology ; Amitriptyline/metabolism ; Choline ; Diet ; Disease Models, Animal ; Liver/metabolism ; Methionine/metabolism ; Mice, Inbred C57BL ; Mice, Knockout ; Non-alcoholic Fatty Liver Disease/genetics ; Non-alcoholic Fatty Liver Disease/metabolism ; Racemethionine/metabolism ; Sphingomyelin Phosphodiesterase/genetics ; Sphingomyelin Phosphodiesterase/metabolism ; Hepatitis/metabolism
    Chemical Substances Amitriptyline (1806D8D52K) ; Choline (N91BDP6H0X) ; Methionine (AE28F7PNPL) ; Racemethionine (73JWT2K6T3) ; Sphingomyelin Phosphodiesterase (EC 3.1.4.12)
    Language English
    Publishing date 2023-01-02
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701011-9
    ISSN 2213-2317 ; 2213-2317
    ISSN (online) 2213-2317
    ISSN 2213-2317
    DOI 10.1016/j.redox.2022.102596
    Database MEDical Literature Analysis and Retrieval System OnLINE

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