What have we learned from animal models of idiosyncratic, drug-induced liver injury?

Roth, Robert A.; Ganey, Patricia E.

doi:10.1080/17425255.2020.1760246

Cited by 8Drug-Induced Hepatotoxicity and ProtectionDrug-Induced Adverse ReactionsImmunotoxicology and immune responses

What have we learned from animal models of idiosyncratic, drug-induced liver injury?

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Roth, Robert A., Ganey, Patricia E.·2020·Expert Opinion on Drug Metabolism & Toxicology

DOI 10.1080/17425255.2020.1760246PMC PMC7315440

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Abstract

INTRODUCTION: Idiosyncratic, drug-induced liver injury (IDILI) continues to plague patients and restrict the use of drugs that are pharmacologically effective. Mechanisms of IDILI are incompletely understood, and a better understanding would reduce speculation and could help to identify safer drug candidates preclinically. Animal models have the potential to enhance knowledge of mechanisms of IDILI. AREAS COVERED: Numerous hypotheses have emerged to explain IDILI pathogenesis, many of which center on the roles of the innate and/or adaptive immune systems. Animal models based on these hypotheses are reviewed in the context of their contributions to understanding of IDILI and their limitations. EXPERT OPINION: Animal models of IDILI based on an activated adaptive immune system have to date failed to reproduce major liver injury that is of most concern clinically. The only models that have so far resulted in pronounced liver injury are based on the multiple determinant hypothesis or the inflammatory stress hypothesis. The liver pathogenesis in IDILI animal models involves various leukocytes and immune mediators such as cytokines. Insights from animal models are changing the way we view IDILI pathogenesis and are leading to better approaches to preclinical prediction of IDILI potential of new drug candidates.

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The role of an activated immune system is considered to contribute to idiosyncratic DILI where a reactive metabolite forms an adduct that behaves like a hapten to activate the adaptive immune system or directly activates innate immune cells to increase inflammatory cytokine production such as TNFα.
“The role of an activated immune system is considered to contribute to idiosyncratic DILI where a reactive metabolite forms an adduct that behaves like a hapten to activate the adaptive immune system40 or directly activates innate immune cells (e.g., Kupffer cell) to increase inflammatory cytokine production such as TNFα41.”
From Performance assessment and economic analysis of a human Liver-Chip for predictive toxicology (2022) · cites this paper as [41]
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Authors: Roth, R. A., & Ganey, P. E.
Affiliations: Michigan State University (US)
Corresponding author: Roth, Robert A.
Venue: Expert Opinion on Drug Metabolism & Toxicology
Publisher: Informa UK Limited
Published: 2020-05-04
Volume: 16
Issue: 6
Pages: 475-491
ISSN: 1742-5255 (ISSN-L)
1744-7607
DOI: 10.1080/17425255.2020.1760246
PMC: PMC7315440
OpenAlex: W3017979272
Cited by: 8
References: 126
Citations by year: 2026: 2 · 2025: 1 · 2024: 2 · 2022: 2 · 2021: 1
FWCI: 0.13
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Expert Opinion on Drug Metabolism & Toxicology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institute for Diabetes and Digestive and Kidney Diseases (R01DK112695)
Topics: Life Sciences › Pharmacology, Toxicology and Pharmaceutics › Pharmacology › Drug-Induced Hepatotoxicity and Protection
Health Sciences › Medicine › Pharmacology › Drug-Induced Adverse Reactions
Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
Keywords: idiosyncratic drug-induced liver injury, animal models, adaptive immunity, innate immune system, cytokines, leukocytes, drug safety
MeSH terms: Animals, Disease Models, Animal, Drug Evaluation, Preclinical, Humans, Immunity, Innate, Cytokines, Chemical and Drug Induced Liver Injury, Adaptive Immunity

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What have we learned from animal models of idiosyncratic, drug-induced liver injury?

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