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  1. Article ; Online: Crosstalk between Oxidative Stress and Inflammatory Liver Injury in the Pathogenesis of Alcoholic Liver Disease

    Yoon Mee Yang / Ye Eun Cho / Seonghwan Hwang

    International Journal of Molecular Sciences, Vol 23, Iss 774, p

    2022  Volume 774

    Abstract: Alcoholic liver disease (ALD) is characterized by the injury, inflammation, and scarring in the liver owing to excessive alcohol consumption. Currently, ALD is a leading cause for liver transplantation. Therefore, extensive studies (in vitro, in ... ...

    Abstract Alcoholic liver disease (ALD) is characterized by the injury, inflammation, and scarring in the liver owing to excessive alcohol consumption. Currently, ALD is a leading cause for liver transplantation. Therefore, extensive studies (in vitro, in experimental ALD models and in humans) are needed to elucidate pathological features and pathogenic mechanisms underlying ALD. Notably, oxidative changes in the liver have been recognized as a signature trait of ALD. Progression of ALD is linked to the generation of highly reactive free radicals by reactions involving ethanol and its metabolites. Furthermore, hepatic oxidative stress promotes tissue injury and, in turn, stimulates inflammatory responses in the liver, forming a pathological loop that promotes the progression of ALD. Accordingly, accumulating further knowledge on the relationship between oxidative stress and inflammation may help establish a viable therapeutic approach for treating ALD.
    Keywords alcoholic liver disease ; oxidative stress ; inflammatory liver injury ; fatty liver ; alcoholic steatohepatitis ; cirrhosis ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 610
    Language English
    Publishing date 2022-01-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Hepatokines and Non-Alcoholic Fatty Liver Disease

    Tae Hyun Kim / Dong-Gyun Hong / Yoon Mee Yang

    Biomedicines, Vol 9, Iss 1903, p

    Linking Liver Pathophysiology to Metabolism

    2021  Volume 1903

    Abstract: The liver plays a key role in maintaining energy homeostasis by sensing and responding to changes in nutrient status under various metabolic conditions. Recently highlighted as a major endocrine organ, the contribution of the liver to systemic glucose ... ...

    Abstract The liver plays a key role in maintaining energy homeostasis by sensing and responding to changes in nutrient status under various metabolic conditions. Recently highlighted as a major endocrine organ, the contribution of the liver to systemic glucose and lipid metabolism is primarily attributed to signaling crosstalk between multiple organs via hepatic hormones, cytokines, and hepatokines. Hepatokines are hormone-like proteins secreted by hepatocytes, and a number of these have been associated with extra-hepatic metabolic regulation. Mounting evidence has revealed that the secretory profiles of hepatokines are significantly altered in non-alcoholic fatty liver disease (NAFLD), the most common hepatic manifestation, which frequently precedes other metabolic disorders, including insulin resistance and type 2 diabetes. Therefore, deciphering the mechanism of hepatokine-mediated inter-organ communication is essential for understanding the complex metabolic network between tissues, as well as for the identification of novel diagnostic and/or therapeutic targets in metabolic disease. In this review, we describe the hepatokine-driven inter-organ crosstalk in the context of liver pathophysiology, with a particular focus on NAFLD progression. Moreover, we summarize key hepatokines and their molecular mechanisms of metabolic control in non-hepatic tissues, discussing their potential as novel biomarkers and therapeutic targets in the treatment of metabolic diseases.
    Keywords ANGPTL ; energy metabolism ; Fetuin ; FGF21 ; inter-organ communication ; Biology (General) ; QH301-705.5
    Subject code 570
    Language English
    Publishing date 2021-12-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Gα12/13 signaling in metabolic diseases

    Yoon Mee Yang / Da-Sol Kuen / Yeonseok Chung / Hitoshi Kurose / Sang Geon Kim

    Experimental and Molecular Medicine, Vol 52, Iss 6, Pp 896-

    2020  Volume 910

    Abstract: Metabolic diseases: Going after G proteins Understanding the activities of two members of a vital category of proteins called G proteins, which initiate metabolic changes when signaling molecules bind to cells, could lead to new therapies for many ... ...

    Abstract Metabolic diseases: Going after G proteins Understanding the activities of two members of a vital category of proteins called G proteins, which initiate metabolic changes when signaling molecules bind to cells, could lead to new therapies for many diseases. Researchers in South Korea and Japan, led by Sang Geon Kim at Seoul National University, review the significance of the Gα12 and Gα13 proteins in diseases characterised by significant changes in metabolism, including liver conditions and disorders of the cardiovascular and immune systems. Specific roles for the proteins have been identified by a variety of methods, including studying the effect of disabling the genes that code for them in mice. Recent insights suggest that drugs interfering with the activity of these Gα proteins might help treat many conditions in which the molecular signalling networks involving the proteins are disrupted.
    Keywords Medicine ; R ; Biochemistry ; QD415-436
    Language English
    Publishing date 2020-06-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: AMPK-associated signaling to bridge the gap between fuel metabolism and hepatocyte viability

    Yoon Mee Yang, Chang Yeob Han, Yoon Jun Kim, Sang Geon Kim

    World Journal of Gastroenterology, Vol 16, Iss 30, Pp 3731-

    2010  Volume 3742

    Abstract: The adenosine monophosphate-activated protein kinase (AMPK) and p70 ribosomal S6 kinase-1 pathway may serve as a key signaling flow that regulates energy metabolism; thus, this pathway becomes an attractive target for the treatment of liver diseases that ...

    Abstract The adenosine monophosphate-activated protein kinase (AMPK) and p70 ribosomal S6 kinase-1 pathway may serve as a key signaling flow that regulates energy metabolism; thus, this pathway becomes an attractive target for the treatment of liver diseases that result from metabolic derangements. In addition, AMPK emerges as a kinase that controls the redox-state and mitochondrial function, whose activity may be modulated by antioxidants. A close link exists between fuel metabolism and mitochondrial biogenesis. The relationship between fuel metabolism and cell survival strongly implies the existence of a shared signaling network, by which hepatocytes respond to challenges of external stimuli. The AMPK pathway may belong to this network. A series of drugs and therapeutic candidates enable hepatocytes to protect mitochondria from radical stress and increase cell viability, which may be associated with the activation of AMPK, liver kinase B1, and other molecules or components. Consequently, the components downstream of AMPK may contribute to stabilizing mitochondrial membrane potential for hepatocyte survival. In this review, we discuss the role of the AMPK pathway in hepatic energy metabolism and hepatocyte viability. This information may help identify ways to prevent and/or treat hepatic diseases caused by the metabolic syndrome. Moreover, clinical drugs and experimental therapeutic candidates that directly or indirectly modulate the AMPK pathway in distinct manners are discussed here with particular emphasis on their effects on fuel metabolism and mitochondrial function.
    Keywords Adenosine monophosphate-activated protein kinase ; Cell survival ; Energy metabolism ; Fatty liver ; Insulin resistance ; Glycogen synthase kinase 3β ; p70 ribosomal S6 kinase-1 ; Diseases of the digestive system. Gastroenterology ; RC799-869 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Gastroenterology ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Subject code 571
    Language English
    Publishing date 2010-08-01T00:00:00Z
    Publisher Baishideng Publishing Group Co. Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Transactivation of Genes Encoding for Phase II Enzymes and Phase III Transporters by Phytochemical Antioxidants

    Sang Geon Kim / Kyoung Noh / Yoon Mee Yang / Chang Yeob Han

    Molecules, Vol 15, Iss 9, Pp 6332-

    2010  Volume 6348

    Abstract: The induction of phase II enzymes and phase III transporters contributes to the metabolism, detoxification of xenobiotics, antioxidant capacity, redox homeostasis and cell viability. Transactivation of the genes that encode for phase II enzymes and phase ...

    Abstract The induction of phase II enzymes and phase III transporters contributes to the metabolism, detoxification of xenobiotics, antioxidant capacity, redox homeostasis and cell viability. Transactivation of the genes that encode for phase II enzymes and phase III transporters is coordinatively regulated by activating transcription factors in response to external stimuli. Comprehensive studies indicate that antioxidant phytochemicals promote the induction of phase II enzymes and/or phase III transporters through various signaling pathways, including phosphoinositide 3-kinase, protein kinase C, and mitogen-activated protein kinases. This paper focuses on the molecular mechanisms and signaling pathways responsible for the transactivation of genes encoding for these proteins, as orchestrated by a series of transcription factors and related signaling components.
    Keywords phase 2 enzyme ; phase 3 transporter ; NF-E2-related factor 2 ; CCAAT-enhancer binding protein-b ; hepatic nuclear factor ; farnesoid X receptor ; Organic chemistry ; QD241-441
    Language English
    Publishing date 2010-09-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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