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  1. Article ; Online: Comments on: Unveiling the therapeutic promise of natural products in alleviating drug-induced liver injury: Present advancements and future prospects.

    Jaeschke, Hartmut / Ramachandran, Anup

    Phytotherapy research : PTR

    2024  Volume 38, Issue 4, Page(s) 1781–1782

    MeSH term(s) Humans ; Biological Products/therapeutic use ; Chemical and Drug Induced Liver Injury/drug therapy
    Chemical Substances Biological Products
    Language English
    Publishing date 2024-02-05
    Publishing country England
    Document type Letter
    ZDB-ID 639136-9
    ISSN 1099-1573 ; 0951-418X
    ISSN (online) 1099-1573
    ISSN 0951-418X
    DOI 10.1002/ptr.8145
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  2. Article ; Online: Acetaminophen Hepatotoxicity: Paradigm for Understanding Mechanisms of Drug-Induced Liver Injury.

    Jaeschke, Hartmut / Ramachandran, Anup

    Annual review of pathology

    2024  Volume 19, Page(s) 453–478

    Abstract: Acetaminophen (APAP) overdose is the clinically most relevant drug hepatotoxicity in western countries, and, because of translational relevance of animal models, APAP is mechanistically the most studied drug. This review covers intracellular signaling ... ...

    Abstract Acetaminophen (APAP) overdose is the clinically most relevant drug hepatotoxicity in western countries, and, because of translational relevance of animal models, APAP is mechanistically the most studied drug. This review covers intracellular signaling events starting with drug metabolism and the central role of mitochondrial dysfunction involving oxidant stress and peroxynitrite. Mitochondria-derived endonucleases trigger nuclear DNA fragmentation, the point of no return for cell death. In addition, adaptive mechanisms that limit cell death are discussed including autophagy, mitochondrial morphology changes, and biogenesis. Extensive evidence supports oncotic necrosis as the mode of cell death; however, a partial overlap with signaling events of apoptosis, ferroptosis, and pyroptosis is the basis for controversial discussions. Furthermore, an update on sterile inflammation in injury and repair with activation of Kupffer cells, monocyte-derived macrophages, and neutrophils is provided. Understanding these mechanisms of cell death led to discovery of
    MeSH term(s) Humans ; Animals ; Acetaminophen/adverse effects ; Chemical and Drug Induced Liver Injury/etiology ; Apoptosis ; Acetylcysteine/pharmacology ; Acetylcysteine/therapeutic use ; Autophagy
    Chemical Substances Acetaminophen (362O9ITL9D) ; Acetylcysteine (WYQ7N0BPYC)
    Language English
    Publishing date 2024-01-24
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2227429-7
    ISSN 1553-4014 ; 1553-4006
    ISSN (online) 1553-4014
    ISSN 1553-4006
    DOI 10.1146/annurev-pathmechdis-051122-094016
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  3. Article ; Online: Mitochondria in Acetaminophen-Induced Liver Injury and Recovery

    Anup Ramachandran / Hartmut Jaeschke

    Livers, Vol 3, Iss 14, Pp 219-

    A Concise Review

    2023  Volume 231

    Abstract: Mitochondria are critical organelles responsible for the maintenance of cellular energy homeostasis. Thus, their dysfunction can have severe consequences in cells responsible for energy-intensive metabolic function, such as hepatocytes. Extensive ... ...

    Abstract Mitochondria are critical organelles responsible for the maintenance of cellular energy homeostasis. Thus, their dysfunction can have severe consequences in cells responsible for energy-intensive metabolic function, such as hepatocytes. Extensive research over the last decades have identified compromised mitochondrial function as a central feature in the pathophysiology of liver injury induced by an acetaminophen (APAP) overdose, the most common cause of acute liver failure in the United States. While hepatocyte mitochondrial oxidative and nitrosative stress coupled with induction of the mitochondrial permeability transition are well recognized after an APAP overdose, recent studies have revealed additional details about the organelle’s role in APAP pathophysiology. This concise review highlights these new advances, which establish the central role of the mitochondria in APAP pathophysiology, and places them in the context of earlier information in the literature. Adaptive alterations in mitochondrial morphology as well as the role of cellular iron in mitochondrial dysfunction and the organelle’s importance in liver recovery after APAP-induced injury will be discussed.
    Keywords acetaminophen ; mitochondria ; paracetamol ; iron ; morphology ; spheroid ; Medicine (General) ; R5-920
    Subject code 610
    Language English
    Publishing date 2023-04-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Mitochondria in Acetaminophen-Induced Liver Injury and Recovery: A Concise Review.

    Ramachandran, Anup / Jaeschke, Hartmut

    Livers

    2023  Volume 3, Issue 2, Page(s) 219–231

    Abstract: Mitochondria are critical organelles responsible for the maintenance of cellular energy homeostasis. Thus, their dysfunction can have severe consequences in cells responsible for energy-intensive metabolic function, such as hepatocytes. Extensive ... ...

    Abstract Mitochondria are critical organelles responsible for the maintenance of cellular energy homeostasis. Thus, their dysfunction can have severe consequences in cells responsible for energy-intensive metabolic function, such as hepatocytes. Extensive research over the last decades have identified compromised mitochondrial function as a central feature in the pathophysiology of liver injury induced by an acetaminophen (APAP) overdose, the most common cause of acute liver failure in the United States. While hepatocyte mitochondrial oxidative and nitrosative stress coupled with induction of the mitochondrial permeability transition are well recognized after an APAP overdose, recent studies have revealed additional details about the organelle's role in APAP pathophysiology. This concise review highlights these new advances, which establish the central role of the mitochondria in APAP pathophysiology, and places them in the context of earlier information in the literature. Adaptive alterations in mitochondrial morphology as well as the role of cellular iron in mitochondrial dysfunction and the organelle's importance in liver recovery after APAP-induced injury will be discussed.
    Language English
    Publishing date 2023-04-10
    Publishing country Switzerland
    Document type Journal Article
    ISSN 2673-4389
    ISSN (online) 2673-4389
    DOI 10.3390/livers3020014
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  5. Article ; Online: Central mechanisms of acetaminophen hepatotoxicity: mitochondrial dysfunction by protein adducts and oxidant stress.

    Jaeschke, Hartmut / Ramachandran, Anup

    Drug metabolism and disposition: the biological fate of chemicals

    2023  

    Abstract: Acetaminophen (APAP) is an analgesic and antipyretic drug used worldwide, which is safe at therapeutic doses. However, an overdose can induce liver injury and even liver failure. Mechanistic studies in mice beginning with the seminal papers published by ... ...

    Abstract Acetaminophen (APAP) is an analgesic and antipyretic drug used worldwide, which is safe at therapeutic doses. However, an overdose can induce liver injury and even liver failure. Mechanistic studies in mice beginning with the seminal papers published by B.B. Brodie's group in the 1970s have resulted in important insight into the pathophysiology. Although the metabolic activation of APAP with generation of a reactive metabolite, glutathione depletion and protein adduct formation are critical initiating events, more recently the mitochondria came into focus as important target and decision point of cell death. This review provides a comprehensive overview of the induction of mitochondrial superoxide and peroxynitrite formation and its propagation through a mitogen activated protein kinase cascade, the mitochondrial permeability transition pore opening caused by iron-catalyzed protein nitration and the mitochondria-dependent nuclear DNA fragmentation. In addition, the role of adaptive mechanisms that can modulate the pathophysiology including autophagy, mitophagy, Nrf2 activation and mitochondrial biogenesis, are discussed. Importantly, it is outlined how the mechanisms elucidated in mice translate to human hepatocytes and APAP overdose patients, and how this mechanistic insight explains the mechanism of action of the clinically approved antidote
    Language English
    Publishing date 2023-08-11
    Publishing country United States
    Document type Journal Article
    ZDB-ID 186795-7
    ISSN 1521-009X ; 0090-9556
    ISSN (online) 1521-009X
    ISSN 0090-9556
    DOI 10.1124/dmd.123.001279
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  6. Article ; Online: Putative Effects of an Orally Administered Anti-TLR4 Antibody on Gut Microbiota and Acetaminophen Hepatotoxicity in Mice.

    Jaeschke, Hartmut / Ramachandran, Anup

    Microbiology spectrum

    2022  Volume 11, Issue 1, Page(s) e0186322

    MeSH term(s) Animals ; Mice ; Acetaminophen/toxicity ; Chemical and Drug Induced Liver Injury ; Drug-Related Side Effects and Adverse Reactions ; Gastrointestinal Microbiome ; Liver/pathology ; Toll-Like Receptor 4/immunology ; Antibodies/pharmacology
    Chemical Substances Acetaminophen (362O9ITL9D) ; Toll-Like Receptor 4 ; Antibodies
    Language English
    Publishing date 2022-12-13
    Publishing country United States
    Document type Letter ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2807133-5
    ISSN 2165-0497 ; 2165-0497
    ISSN (online) 2165-0497
    ISSN 2165-0497
    DOI 10.1128/spectrum.01863-22
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  7. Article ; Online: Does acetaminophen hepatotoxicity involve apoptosis, inflammatory liver injury, and lipid peroxidation?

    Jaeschke, Hartmut / Ramachandran, Anup

    Journal of biochemical and molecular toxicology

    2021  Volume 35, Issue 2, Page(s) e22718

    Language English
    Publishing date 2021-01-23
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 1410020-4
    ISSN 1099-0461 ; 1095-6670
    ISSN (online) 1099-0461
    ISSN 1095-6670
    DOI 10.1002/jbt.22718
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  8. Article ; Online: Targeting the sterile inflammatory response during acetaminophen hepatotoxicity with natural products.

    Jaeschke, Hartmut / Ramachandran, Anup

    Toxicology letters

    2021  Volume 355, Page(s) 170–171

    MeSH term(s) Acetaminophen ; Analgesics, Non-Narcotic ; Biological Products ; Chemical and Drug Induced Liver Injury ; Humans
    Chemical Substances Analgesics, Non-Narcotic ; Biological Products ; Acetaminophen (362O9ITL9D)
    Language English
    Publishing date 2021-11-18
    Publishing country Netherlands
    Document type Letter ; Comment
    ZDB-ID 433788-8
    ISSN 1879-3169 ; 0378-4274
    ISSN (online) 1879-3169
    ISSN 0378-4274
    DOI 10.1016/j.toxlet.2021.11.006
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  9. Article ; Online: Oxidant Stress and Acetaminophen Hepatotoxicity: Mechanism-Based Drug Development.

    Ramachandran, Anup / Jaeschke, Hartmut

    Antioxidants & redox signaling

    2021  Volume 35, Issue 9, Page(s) 718–733

    Abstract: Significance: ...

    Abstract Significance:
    MeSH term(s) Acetaminophen/adverse effects ; Animals ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/metabolism ; Drug Development ; Humans ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Oxidants/metabolism ; Oxidative Stress
    Chemical Substances Oxidants ; Acetaminophen (362O9ITL9D)
    Language English
    Publishing date 2021-07-07
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 1483836-9
    ISSN 1557-7716 ; 1523-0864
    ISSN (online) 1557-7716
    ISSN 1523-0864
    DOI 10.1089/ars.2021.0102
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  10. Article ; Online: The p21

    Umbaugh, David S / Nguyen, Nga T / Smith, Sawyer H / Ramachandran, Anup / Jaeschke, Hartmut

    Toxicology

    2024  Volume 504, Page(s) 153804

    Abstract: Fifty percent of all acute liver failure (ALF) cases in the United States are due to acetaminophen (APAP) overdose. Assessment of canonical features of liver injury, such as plasma alanine aminotransferase activities are poor predictors of acute liver ... ...

    Abstract Fifty percent of all acute liver failure (ALF) cases in the United States are due to acetaminophen (APAP) overdose. Assessment of canonical features of liver injury, such as plasma alanine aminotransferase activities are poor predictors of acute liver failure (ALF), suggesting the involvement of additional mechanisms independent of hepatocyte death. Previous work demonstrated a severe overdose of APAP results in impaired regeneration, the induction of senescence by p21, and increased mortality. We hypothesized that a discrete population of p21
    MeSH term(s) Acetaminophen/toxicity ; Animals ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Hepatocytes/pathology ; Humans ; Male ; Chemical and Drug Induced Liver Injury/pathology ; Chemical and Drug Induced Liver Injury/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/metabolism ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; Female ; Mice ; Chemokines, CXC/metabolism ; Chemokines, CXC/genetics ; Mice, Inbred C57BL ; Liver Regeneration/drug effects ; Drug Overdose ; Analgesics, Non-Narcotic/toxicity
    Chemical Substances Acetaminophen (362O9ITL9D) ; Cyclin-Dependent Kinase Inhibitor p21 ; Chemokines, CXC ; CXCL14 protein, mouse ; CXCL14 protein, human ; Cdkn1a protein, mouse ; Analgesics, Non-Narcotic ; CDKN1A protein, human
    Language English
    Publishing date 2024-04-12
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 184557-3
    ISSN 1879-3185 ; 0300-483X
    ISSN (online) 1879-3185
    ISSN 0300-483X
    DOI 10.1016/j.tox.2024.153804
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