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  1. Article ; Online: Introducing the Editorial Fellow and the Fellows' Corner.

    Malhi, Harmeet / Gores, Gregory J

    Hepatology (Baltimore, Md.)

    2023  Volume 78, Issue 6, Page(s) 1677

    MeSH term(s) Education, Medical, Graduate ; Curriculum ; Fellowships and Scholarships ; Surveys and Questionnaires ; Clinical Competence
    Language English
    Publishing date 2023-11-16
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1097/HEP.0000000000000680
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Foreseeing Alcohol-Associated Liver Disease through Proteomic Biomarkers.

    Daniel, P Vineeth / Malhi, Harmeet

    Clinical chemistry

    2023  Volume 69, Issue 5, Page(s) 438–441

    MeSH term(s) Humans ; Proteomics ; Biomarkers ; Liver ; Liver Diseases ; Liver Diseases, Alcoholic/diagnosis
    Chemical Substances Biomarkers
    Language English
    Publishing date 2023-01-04
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 80102-1
    ISSN 1530-8561 ; 0009-9147
    ISSN (online) 1530-8561
    ISSN 0009-9147
    DOI 10.1093/clinchem/hvac177
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Letters to the Editor: defining utility and pertinence.

    Malhi, Harmeet / Gores, Gregory J

    Hepatology (Baltimore, Md.)

    2023  Volume 77, Issue 4, Page(s) 1069–1070

    Language English
    Publishing date 2023-02-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1097/HEP.0000000000000318
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: What is Hepatology looking for version 2.0?

    Malhi, Harmeet / Gores, Gregory J

    Hepatology (Baltimore, Md.)

    2023  Volume 77, Issue 3, Page(s) 707–708

    Language English
    Publishing date 2023-02-17
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.32637
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  5. Article ; Online: Emerging role of extracellular vesicles in liver diseases.

    Malhi, Harmeet

    American journal of physiology. Gastrointestinal and liver physiology

    2019  Volume 317, Issue 5, Page(s) G739–G749

    Abstract: Extracellular vesicles (EVs) are membrane-defined nanoparticles released by most cell types. The EVs released by cells may differ quantitatively and qualitatively from physiological states to disease states. There are several unique properties of EVs, ... ...

    Abstract Extracellular vesicles (EVs) are membrane-defined nanoparticles released by most cell types. The EVs released by cells may differ quantitatively and qualitatively from physiological states to disease states. There are several unique properties of EVs, including their proteins, lipids and nucleic acid cargoes, stability in circulation, and presence in biofluids, which make them a critical vector for cell-to-cell communication and impart utility as a biomarker. EVs may also serve as a vehicle for selective cargo secretion. Similarly, EV cargo may be selectively manipulated for targeted therapeutic delivery. In this review an overview is provided on the EV classification, biogenesis, and secretion pathways, which are conserved across cell types. Next, cargo characterization and effector cell responses are discussed in the context of nonalcoholic steatohepatitis, alcoholic hepatitis, and acetaminophen-induced liver injury. The review also discusses the potential biomarker and therapeutic uses of circulating EVs.
    MeSH term(s) Animals ; Biomarkers/metabolism ; Extracellular Vesicles/classification ; Extracellular Vesicles/metabolism ; Extracellular Vesicles/transplantation ; Humans ; Lipid Metabolism ; Liver Diseases/diagnosis ; Liver Diseases/metabolism ; Liver Diseases/therapy ; Secretory Pathway
    Chemical Substances Biomarkers
    Language English
    Publishing date 2019-09-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 603840-2
    ISSN 1522-1547 ; 0193-1857
    ISSN (online) 1522-1547
    ISSN 0193-1857
    DOI 10.1152/ajpgi.00183.2019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Assessment of Lipotoxic Endoplasmic Reticulum (ER) Stress in Nonalcoholic Steatohepatitis (NASH).

    Parthasarathy, Gopanandan / Malhi, Harmeet

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2455, Page(s) 243–254

    Abstract: Hepatocyte lipotoxicity is a hallmark of nonalcoholic steatohepatitis (NASH), and lipid induced liver injury occurs, in part, via activation of endoplasmic reticulum (ER) stress. Consequently, the unfolded protein response (UPR) is initiated, driven by ... ...

    Abstract Hepatocyte lipotoxicity is a hallmark of nonalcoholic steatohepatitis (NASH), and lipid induced liver injury occurs, in part, via activation of endoplasmic reticulum (ER) stress. Consequently, the unfolded protein response (UPR) is initiated, driven by three key ER transmembrane proteins, resulting in downstream responses that are dynamic and interconnected. Thus, careful interrogation of these pathways is required to investigate the complex role of ER stress in NASH. Herein, we describe different mechanisms of, and in vitro assays for assessment of lipotoxic ER stress in mouse hepatocytes.
    MeSH term(s) Animals ; Apoptosis ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum Stress/physiology ; Hepatocytes/metabolism ; Liver/metabolism ; Mice ; Non-alcoholic Fatty Liver Disease/metabolism
    Language English
    Publishing date 2022-02-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-2128-8_19
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Manuscript best practices: Takeaways from a community conversation.

    Wong, Carmen Chak-Lui / Tapper, Elliot B / Malhi, Harmeet / Gores, Gregory J

    Hepatology (Baltimore, Md.)

    2024  

    Language English
    Publishing date 2024-03-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1097/HEP.0000000000000849
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The Role of Endoplasmic Reticulum in Lipotoxicity during Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) Pathogenesis.

    Venkatesan, Nanditha / Doskey, Luke C / Malhi, Harmeet

    The American journal of pathology

    2023  Volume 193, Issue 12, Page(s) 1887–1899

    Abstract: Perturbations in lipid and protein homeostasis induce endoplasmic reticulum (ER) stress in metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease. Lipotoxic and proteotoxic stress can activate ...

    Abstract Perturbations in lipid and protein homeostasis induce endoplasmic reticulum (ER) stress in metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease. Lipotoxic and proteotoxic stress can activate the unfolded protein response (UPR) transducers: inositol requiring enzyme1α, PKR-like ER kinase, and activating transcription factor 6α. Collectively, these pathways induce expression of genes that encode functions to resolve the protein folding defect and ER stress by increasing the protein folding capacity of the ER and degradation of misfolded proteins. The ER is also intimately connected with lipid metabolism, including de novo ceramide synthesis, phospholipid and cholesterol synthesis, and lipid droplet formation. Following their activation, the UPR transducers also regulate lipogenic pathways in the liver. With persistent ER stress, cellular adaptation fails, resulting in hepatocyte apoptosis, a pathological marker of liver disease. In addition to the ER-nucleus signaling activated by the UPR, the ER can interact with other organelles via membrane contact sites. Modulating intracellular communication between ER and endosomes, lipid droplets, and mitochondria to restore ER homeostasis could have therapeutic efficacy in ameliorating liver disease. Recent studies have also demonstrated that cells can convey ER stress by the release of extracellular vesicles. This review discusses lipotoxic ER stress and the central role of the ER in communicating ER stress to other intracellular organelles in MASLD pathogenesis.
    MeSH term(s) Humans ; Endoplasmic Reticulum Stress/physiology ; Unfolded Protein Response ; Non-alcoholic Fatty Liver Disease/metabolism ; Endoplasmic Reticulum/metabolism
    Language English
    Publishing date 2023-09-07
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2943-9
    ISSN 1525-2191 ; 0002-9440
    ISSN (online) 1525-2191
    ISSN 0002-9440
    DOI 10.1016/j.ajpath.2023.08.007
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  9. Article ; Online: Thematic reviews: The future of hepatology.

    Malhi, Harmeet / Shah, Vijay / Gores, Gregory J

    Hepatology (Baltimore, Md.)

    2023  Volume 78, Issue 2, Page(s) 388

    MeSH term(s) Gastroenterology ; Forecasting
    Language English
    Publishing date 2023-04-19
    Publishing country United States
    Document type Research Support, Non-U.S. Gov't ; Editorial ; Research Support, N.I.H., Extramural
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1097/HEP.0000000000000409
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Emerging targets for therapy in ALD: Lessons from NASH.

    Singal, Ashwani K / Shah, Vijay H / Malhi, Harmeet

    Hepatology (Baltimore, Md.)

    2023  

    Abstract: Alcohol-associated liver disease due to harmful alcohol use and NAFLD associated with metabolic syndrome are the 2 most common liver diseases worldwide. Control of respective risk factors is the cornerstone in the long-term management of these diseases. ... ...

    Abstract Alcohol-associated liver disease due to harmful alcohol use and NAFLD associated with metabolic syndrome are the 2 most common liver diseases worldwide. Control of respective risk factors is the cornerstone in the long-term management of these diseases. Furthermore, there are no effective therapies. Both diseases are characterized by metabolic derangements; thus, the focus of this review was to broaden our understanding of metabolic targets investigated in NAFLD, and how these can be applied to alcohol-associated liver disease. Conserved pathogenic pathways such as dysregulated lipid metabolism, cell death pathways including apoptosis and activation of innate immune cells, and stellate cells mediate both alcohol and NAFLDs, resulting in histological abnormalities of steatosis, inflammation, fibrosis, and cirrhosis. However, pathways such as gut microbiome changes, glucose metabolism and insulin resistance, inflammatory signaling, and microRNA abnormalities are distinct in these 2 diseases. In this review article, we describe conserved and distinct pathogenic pathways highlighting therapeutic targets that may be of potential in both diseases and those that are unique to each disease.
    Language English
    Publishing date 2023-03-21
    Publishing country United States
    Document type Journal Article
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1097/HEP.0000000000000381
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