LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 128

Search options

  1. Article ; Online: Elucidating the role of extracellular vesicles in liver injury induced by HIV.

    Osna, Natalia A / Poluektova, Larisa Y

    Expert review of gastroenterology & hepatology

    2023  Volume 17, Issue 7, Page(s) 701–708

    Abstract: Introduction: Liver disease is known as one of the leading co-morbidities in HIV infection, with 18% of non-AIDS-related mortality. There is constant crosstalk between liver parenchymal (hepatocytes) and non-parenchymal cells (macrophages, hepatic ... ...

    Abstract Introduction: Liver disease is known as one of the leading co-morbidities in HIV infection, with 18% of non-AIDS-related mortality. There is constant crosstalk between liver parenchymal (hepatocytes) and non-parenchymal cells (macrophages, hepatic stellate cells, endothelial cells), and extracellular vesicles (EVs) are one of the most important ways of cell-to-cell communication.
    Areas covered: We briefly cover the role of EVs in liver disease as well as what is known about the role of small EVs, exosomes, in HIV-induced liver disease potentiated by alcohol as one of the second hits. We also touch large EVs, apoptotic bodies (ABs), in HIV-induced liver injury, the mechanisms of their formation and potentiation by second hits, and their role in the progression of liver disease.
    Expert opinion/commentary: Liver cells are an important source of EVs, which may provide the connection between different organs via secretion into the circulating blood (exosomes) or serve for the communication between the cells within the organ (ABs). Understanding the role of liver EVs in HIV infection and the involvement of second hits in EV generation would provide a new angle for the analysis of HIV-related liver disease pathogenesis and progression to end-stage liver disease.
    MeSH term(s) Humans ; HIV Infections/complications ; Endothelial Cells ; Extracellular Vesicles ; Liver Diseases/etiology
    Language English
    Publishing date 2023-07-03
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2481021-6
    ISSN 1747-4132 ; 1747-4124
    ISSN (online) 1747-4132
    ISSN 1747-4124
    DOI 10.1080/17474124.2023.2230867
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article: Editorial: Cell-to-cell communications in alcohol-associated, metabolic-related and viral liver diseases.

    Osna, Natalia A / Sherman, Kenneth E / Mandrekar, Pranoti / Kharbanda, Kusum K

    Frontiers in physiology

    2023  Volume 14, Page(s) 1269042

    Language English
    Publishing date 2023-10-10
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2023.1269042
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article: Editorial: Alcohol-associated liver disease-From pathogenesis to treatment.

    Kharbanda, Kusum K / Singal, Ashwani K / Mueller, Sebastian / Osna, Natalia A

    Frontiers in physiology

    2022  Volume 13, Page(s) 1060812

    Language English
    Publishing date 2022-10-20
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2564217-0
    ISSN 1664-042X
    ISSN 1664-042X
    DOI 10.3389/fphys.2022.1060812
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article ; Online: Effect of cofactors on NAFLD/NASH and MAFLD. A paradigm illustrating the pathomechanics of organ dysfunction.

    Lonardo, Amedeo / Singal, Ashwani K / Osna, Natalia / Kharbanda, Kusum K

    Metabolism and target organ damage

    2022  Volume 2, Issue 3

    Abstract: Primary nonalcoholic fatty liver disease (NAFLD) is bi-directionally associated with the metabolic syndrome and its constitutive features ("factors": impaired glucose disposal, visceral obesity, arterial hypertension, and dyslipidemia). Secondary NAFLD ... ...

    Abstract Primary nonalcoholic fatty liver disease (NAFLD) is bi-directionally associated with the metabolic syndrome and its constitutive features ("factors": impaired glucose disposal, visceral obesity, arterial hypertension, and dyslipidemia). Secondary NAFLD occurs due to endocrinologic disturbances or other cofactors. This nosography tends to be outdated by the novel definition of metabolic associated fatty liver disease (MAFLD). Irrespective of nomenclature, this condition exhibits a remarkable pathogenic heterogeneity with unpredictable clinical outcomes which are heavily influenced by liver histology changes. Genetics and epigenetics, lifestyle habits [including diet and physical (in)activity] and immunity/infection appear to be major cofactors that modulate NAFLD/MAFLD outcomes, including organ dysfunction owing to liver cirrhosis and hepatocellular carcinoma, type 2 diabetes, chronic kidney disease, heart failure, and sarcopenia. The identification of cofactors for organ dysfunction that may help understand disease heterogeneity and reliably support inherently personalized medicine approaches is a research priority, thus paving the way for innovative treatment strategies.
    Language English
    Publishing date 2022-08-22
    Publishing country United States
    Document type Journal Article
    ISSN 2769-6375
    ISSN (online) 2769-6375
    DOI 10.20517/mtod.2022.14
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article: Pathogenesis of Alcohol-Associated Liver Disease.

    Osna, Natalia A / Rasineni, Karuna / Ganesan, Murali / Donohue, Terrence M / Kharbanda, Kusum K

    Journal of clinical and experimental hepatology

    2022  Volume 12, Issue 6, Page(s) 1492–1513

    Abstract: Excessive alcohol consumption is a global healthcare problem with enormous social, economic, and clinical consequences. While chronic, heavy alcohol consumption causes structural damage and/or disrupts normal organ function in virtually every tissue of ... ...

    Abstract Excessive alcohol consumption is a global healthcare problem with enormous social, economic, and clinical consequences. While chronic, heavy alcohol consumption causes structural damage and/or disrupts normal organ function in virtually every tissue of the body, the liver sustains the greatest damage. This is primarily because the liver is the first to see alcohol absorbed from the gastrointestinal tract via the portal circulation and second, because the liver is the principal site of ethanol metabolism. Alcohol-induced damage remains one of the most prevalent disorders of the liver and a leading cause of death or transplantation from liver disease. Despite extensive research on the pathophysiology of this disease, there are still no targeted therapies available. Given the multifactorial mechanisms for alcohol-associated liver disease pathogenesis, it is conceivable that a multitherapeutic regimen is needed to treat different stages in the spectrum of this disease.
    Language English
    Publishing date 2022-05-31
    Publishing country India
    Document type Journal Article ; Review
    ISSN 0973-6883
    ISSN 0973-6883
    DOI 10.1016/j.jceh.2022.05.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article: A Pathogenic Role of Non-Parenchymal Liver Cells in Alcohol-Associated Liver Disease of Infectious and Non-Infectious Origin.

    Kharbanda, Kusum K / Chokshi, Shilpa / Tikhanovich, Irina / Weinman, Steven A / New-Aaron, Moses / Ganesan, Murali / Osna, Natalia A

    Biology

    2023  Volume 12, Issue 2

    Abstract: Now, much is known regarding the impact of chronic and heavy alcohol consumption on the disruption of physiological liver functions and the induction of structural distortions in the hepatic tissues in alcohol-associated liver disease (ALD). This review ... ...

    Abstract Now, much is known regarding the impact of chronic and heavy alcohol consumption on the disruption of physiological liver functions and the induction of structural distortions in the hepatic tissues in alcohol-associated liver disease (ALD). This review deliberates the effects of alcohol on the activity and properties of liver non-parenchymal cells (NPCs), which are either residential or infiltrated into the liver from the general circulation. NPCs play a pivotal role in the regulation of organ inflammation and fibrosis, both in the context of hepatotropic infections and in non-infectious settings. Here, we overview how NPC functions in ALD are regulated by second hits, such as gender and the exposure to bacterial or viral infections. As an example of the virus-mediated trigger of liver injury, we focused on HIV infections potentiated by alcohol exposure, since this combination was only limitedly studied in relation to the role of hepatic stellate cells (HSCs) in the development of liver fibrosis. The review specifically focusses on liver macrophages, HSC, and T-lymphocytes and their regulation of ALD pathogenesis and outcomes. It also illustrates the activation of NPCs by the engulfment of apoptotic bodies, a frequent event observed when hepatocytes are exposed to ethanol metabolites and infections. As an example of such a double-hit-induced apoptotic hepatocyte death, we deliberate on the hepatotoxic accumulation of HIV proteins, which in combination with ethanol metabolites, causes intensive hepatic cell death and pro-fibrotic activation of HSCs engulfing these HIV- and malondialdehyde-expressing apoptotic hepatocytes.
    Language English
    Publishing date 2023-02-06
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology12020255
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article: Lipidomic Analysis of Liver Lipid Droplets after Chronic Alcohol Consumption with and without Betaine Supplementation.

    Arumugam, Madan Kumar / Perumal, Sathish Kumar / Rasineni, Karuna / Donohue, Terrence M / Osna, Natalia A / Kharbanda, Kusum K

    Biology

    2023  Volume 12, Issue 3

    Abstract: The earliest manifestation of alcohol-associated liver disease is hepatic steatosis, which is characterized by fat accumulation in specialized organelles called lipid droplets (LDs). Our previous studies reported that alcohol consumption elevates the ... ...

    Abstract The earliest manifestation of alcohol-associated liver disease is hepatic steatosis, which is characterized by fat accumulation in specialized organelles called lipid droplets (LDs). Our previous studies reported that alcohol consumption elevates the numbers and sizes of LDs in hepatocytes, which is attenuated by simultaneous treatment with the methyl group donor, betaine. Here, we examined changes in the hepatic lipidome with respect to LD size and dynamics in male Wistar rats fed for 6 weeks with control or ethanol-containing liquid diets that were supplemented with or without 10 mg betaine/mL. At the time of sacrifice, three hepatic LD fractions, LD1 (large droplets), LD2 (medium-sized droplets), and LD3 (small droplets) were isolated from each rat. Untargeted lipidomic analyses revealed that each LD fraction of ethanol-fed rats had higher phospholipids, cholesteryl esters, diacylglycerols, ceramides, and hexosylceramides compared with the corresponding fractions of pair-fed controls. Interestingly, the ratio of phosphatidylcholine to phosphatidylethanolamine (the two most abundant phospholipids on the LD surface) was lower in LD1 fraction compared with LD3 fraction, irrespective of treatment; however, this ratio was significantly lower in ethanol LD fractions compared with their respective control fractions. Betaine supplementation significantly attenuated the ethanol-induced lipidomic changes. These were mainly associated with the regulation of LD surface phospholipids, ceramides, and glycerolipid metabolism in different-sized LD fractions. In conclusion, our results show that ethanol-induced changes in the hepatic LD lipidome likely stabilizes larger-sized LDs during steatosis development. Furthermore, betaine supplementation could effectively reduce the size and dynamics of LDs to attenuate alcohol-associated hepatic steatosis.
    Language English
    Publishing date 2023-03-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2661517-4
    ISSN 2079-7737
    ISSN 2079-7737
    DOI 10.3390/biology12030462
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article ; Online: Increased liver stiffness promotes hepatitis B progression by impairing innate immunity in CCl4-induced fibrotic HBV

    Bybee, Grace / Moeun, Youra / Wang, Weimin / Kharbanda, Kusum K / Poluektova, Larisa Y / Kidambi, Srivatsan / Osna, Natalia A / Ganesan, Murali

    Frontiers in immunology

    2023  Volume 14, Page(s) 1166171

    Abstract: Background: Hepatitis B virus (HBV) infection develops as an acute or chronic liver disease, which progresses from steatosis, hepatitis, and fibrosis to end-stage liver diseases such as cirrhosis and hepatocellular carcinoma (HCC). An increased stromal ... ...

    Abstract Background: Hepatitis B virus (HBV) infection develops as an acute or chronic liver disease, which progresses from steatosis, hepatitis, and fibrosis to end-stage liver diseases such as cirrhosis and hepatocellular carcinoma (HCC). An increased stromal stiffness accompanies fibrosis in chronic liver diseases and is considered a strong predictor for disease progression. The goal of this study was to establish the mechanisms by which enhanced liver stiffness regulates HBV infectivity in the fibrotic liver tissue.
    Methods: For
    Results: We found higher levels of HBV markers in stiff gel-attached hepatocytes accompanied by up-regulated OPN content in cell supernatants as well as suppression of anti-viral interferon-stimulated genes (ISGs). This indicates that pre-requisite "fibrotic" stiffness increases osteopontin (OPN) content and releases and suppresses anti-viral innate immunity, causing a subsequent rise in HBV markers expression in hepatocytes.
    Conclusion: Based on our data, we conclude that liver stiffness enhances OPN levels to limit anti-viral ISG activation in hepatocytes and promote an increase in HBV infectivity, thereby contributing to end-stage liver disease progression.
    MeSH term(s) Mice ; Animals ; Hepatitis B virus ; Mice, Transgenic ; Carcinoma, Hepatocellular ; Liver Neoplasms ; Hepatitis B ; Liver Cirrhosis/chemically induced ; Immunity, Innate ; Hepatitis B Core Antigens ; Hepatitis B Surface Antigens ; Antiviral Agents ; End Stage Liver Disease
    Chemical Substances Hepatitis B Core Antigens ; Hepatitis B Surface Antigens ; Antiviral Agents
    Language English
    Publishing date 2023-08-03
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1166171
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  9. Article ; Online: An annual topic highlight: alcohol and liver, 2011.

    Osna, Natalia A

    World journal of gastroenterology

    2011  Volume 17, Issue 20, Page(s) 2455

    Abstract: AN ANNUAL TOPIC HIGHLIGHT: Alcohol and Liver, 2011, covers the important and new aspects of pathogenesis of alcoholic liver diseases (ALD). It includes broad topics ranging from the exacerbation of ALD by infectious (viral) agents (hepatitis C virus and ... ...

    Abstract AN ANNUAL TOPIC HIGHLIGHT: Alcohol and Liver, 2011, covers the important and new aspects of pathogenesis of alcoholic liver diseases (ALD). It includes broad topics ranging from the exacerbation of ALD by infectious (viral) agents (hepatitis C virus and human immunodeficiency virus) to the influence of alcohol on liver fibrogenesis, lipid rafts, autophagy and other aspects. This issue is recommended for both basic scientists and clinicians who are involved in alcoholic liver research.
    MeSH term(s) Animals ; Biomedical Research/trends ; Disease Models, Animal ; Epigenesis, Genetic/physiology ; Humans ; Liver Cirrhosis/physiopathology ; Liver Diseases, Alcoholic/physiopathology ; Liver Diseases, Alcoholic/therapy ; Liver Diseases, Alcoholic/virology
    Language English
    Publishing date 2011-04-29
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 2185929-2
    ISSN 2219-2840 ; 1007-9327
    ISSN (online) 2219-2840
    ISSN 1007-9327
    DOI 10.3748/wjg.v17.i20.2455
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article ; Online: Multi-Organ Alcohol-Related Damage: Mechanisms and Treatment.

    Osna, Natalia A / Kharbanda, Kusum K

    Biomolecules

    2016  Volume 6, Issue 2

    Abstract: Alcohol consumption causes damage to various organs and systems.[ ... ]. ...

    Abstract Alcohol consumption causes damage to various organs and systems.[...].
    MeSH term(s) Alcohol Dehydrogenase/metabolism ; Cytochrome P-450 CYP2E1/metabolism ; Ethanol/metabolism ; Ethanol/toxicity ; Humans ; Liver/drug effects ; Liver/enzymology ; Liver/injuries ; Oxidative Stress/drug effects
    Chemical Substances Ethanol (3K9958V90M) ; Alcohol Dehydrogenase (EC 1.1.1.1) ; Cytochrome P-450 CYP2E1 (EC 1.14.13.-)
    Language English
    Publishing date 2016-04-15
    Publishing country Switzerland
    Document type Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom6020020
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top