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Article ; Online: Acetaminophen Hepatotoxicity: Not as Simple as One Might Think! Introductory Comments on the Special Issue-

Jaeschke, Hartmut

Livers

2022 Volume 2, Issue 3, Page(s) 105–107

Language	English
Publishing date	2022-07-01
Publishing country	Switzerland
Document type	Journal Article
ISSN	2673-4389
ISSN (online)	2673-4389
DOI	10.3390/livers2030008
Database	MEDical Literature Analysis and Retrieval System OnLINE

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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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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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Article ; Online: Biomarker discovery in acetaminophen hepatotoxicity: leveraging single-cell transcriptomics and mechanistic insight.

Umbaugh, David S / Jaeschke, Hartmut

Expert review of clinical pharmacology

2024 Volume 17, Issue 2, Page(s) 143–155

Abstract: Introduction: Acetaminophen (APAP) overdose is the leading cause of drug-induced liver injury and can cause a rapid progression to acute liver failure (ALF). Therefore, the identification of prognostic biomarkers to determine which patients will require ...

Abstract	Introduction: Acetaminophen (APAP) overdose is the leading cause of drug-induced liver injury and can cause a rapid progression to acute liver failure (ALF). Therefore, the identification of prognostic biomarkers to determine which patients will require a liver transplant is critical for APAP-induced ALF. Areas covered: We begin by relating the mechanistic investigations in mouse models of APAP hepatotoxicity to the human APAP overdose pathophysiology. We draw insights from the established sequence of molecular events in mice to understand the progression of events in the APAP overdose patient. Through this mechanistic understanding, several new biomarkers, such as CXCL14, have recently been evaluated. We also explore how single-cell RNA sequencing, spatial transcriptomics, and other omics approaches have been leveraged for identifying novel biomarkers and how these approaches will continue to push the field of biomarker discovery forward. Expert opinion: Recent investigations have elucidated several new biomarkers or combination of markers such as CXCL14, a regenerative miRNA signature, a cell death miRNA signature, hepcidin, LDH, CPS1, and FABP1. While these biomarkers are promising, they all require further validation. Larger cohort studies analyzing these new biomarkers in the same patient samples, while adding these candidate biomarkers to prognostic models will further support their clinical utility.
MeSH term(s)	Humans ; Mice ; Animals ; Acetaminophen/adverse effects ; Liver Failure, Acute/chemically induced ; MicroRNAs/genetics ; Biomarkers ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/genetics ; Gene Expression Profiling
Chemical Substances	Acetaminophen (362O9ITL9D) ; MicroRNAs ; Biomarkers
Language	English
Publishing date	2024-01-29
Publishing country	England
Document type	Journal Article ; Review
ISSN	1751-2441
ISSN (online)	1751-2441
DOI	10.1080/17512433.2024.2306219
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Article ; Online: Comments on "DNA-binding activities of compounds acting as enzyme inhibitors, ion channel blockers and receptor binders."

Jaeschke, Hartmut

Chemico-biological interactions

2021 Volume 351, Page(s) 109761

Abstract: I read with interest the article "DNA-binding activities of compounds acting as enzyme inhibitors, ion channel blockers and receptor binders" recently published in Chemico-Biological Interactions. The authors suggested that acetaminophen, one of the most ...

Abstract	I read with interest the article "DNA-binding activities of compounds acting as enzyme inhibitors, ion channel blockers and receptor binders" recently published in Chemico-Biological Interactions. The authors suggested that acetaminophen, one of the most used drugs worldwide, alkylates DNA at therapeutic doses and is genotoxic. Given the implications of this statements for public health, it is important for the reader to hear a different perspective that is based on the entire literature on this subject. Everything considered, there is no credible evidence that acetaminophen is a genotoxic hazard or a carcinogen at therapeutic doses.
MeSH term(s)	Acetaminophen ; DNA ; DNA Damage ; Enzyme Inhibitors ; Ion Channels
Chemical Substances	Enzyme Inhibitors ; Ion Channels ; Acetaminophen (362O9ITL9D) ; DNA (9007-49-2)
Language	English
Publishing date	2021-11-26
Publishing country	Ireland
Document type	Letter ; Comment
ZDB-ID	218799-1
ISSN	1872-7786 ; 0009-2797
ISSN (online)	1872-7786
ISSN	0009-2797
DOI	10.1016/j.cbi.2021.109761
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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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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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Article ; Online: Emerging novel therapies against paracetamol (acetaminophen) hepatotoxicity.

Jaeschke, Hartmut

EBioMedicine

2019 Volume 46, Page(s) 9–10

MeSH term(s)	Acetaminophen/administration & dosage ; Acetaminophen/adverse effects ; Animals ; Antidotes/pharmacology ; Antidotes/therapeutic use ; Antipyretics/administration & dosage ; Antipyretics/adverse effects ; Chemical and Drug Induced Liver Injury/etiology ; Chemical and Drug Induced Liver Injury/metabolism ; Chemical and Drug Induced Liver Injury/therapy ; Drug Overdose ; Humans
Chemical Substances	Antidotes ; Antipyretics ; Acetaminophen (362O9ITL9D)
Language	English
Publishing date	2019-07-23
Publishing country	Netherlands
Document type	Letter
ZDB-ID	2851331-9
ISSN	2352-3964
ISSN (online)	2352-3964
DOI	10.1016/j.ebiom.2019.07.054
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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 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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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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