Evidence map›Paper›PMID 38302428›Full record

ReviewDrug metabolism and disposition: the biological fate of chemicals2024

The Discovery of Gut Microbial Metabolites as Modulators of Host Susceptibility to Acetaminophen-Induced Hepatotoxicity.

Hyunwoo Lee, Xiaotong Yang, Pei-Ru Jin, Kyoung-Jae Won, Chang H Kim, Hyunyoung Jeong

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Drug metabolism and disposition: the biological fate of chemicals, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
3.3field-weighted citation impact, top 9% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 7 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Hyunwoo LeeDepartment of Industrial and Molecular Pharmaceutics (H.L., X.Y., P.-R.J., K.-J.W., H.J.), Department of Pharmacy Practice (H.J.), and College of Pharmacy, and Department of Comparative Pathobiology, College of Veterinary Medicine (H.L.), Purdue University, West Lafayette, Indiana and Department of Pathology and Mary H. Weiser Food Allergy Center and Rogel Center for Cancer Research, University of Michigan School of Medicine, Ann Arbor, Michigan (C.H.K.).
Xiaotong YangDepartment of Industrial and Molecular Pharmaceutics (H.L., X.Y., P.-R.J., K.-J.W., H.J.), Department of Pharmacy Practice (H.J.), and College of Pharmacy, and Department of Comparative Pathobiology, College of Veterinary Medicine (H.L.), Purdue University, West Lafayette, Indiana and Department of Pathology and Mary H. Weiser Food Allergy Center and Rogel Center for Cancer Research, University of Michigan School of Medicine, Ann Arbor, Michigan (C.H.K.).
Pei-Ru JinDepartment of Industrial and Molecular Pharmaceutics (H.L., X.Y., P.-R.J., K.-J.W., H.J.), Department of Pharmacy Practice (H.J.), and College of Pharmacy, and Department of Comparative Pathobiology, College of Veterinary Medicine (H.L.), Purdue University, West Lafayette, Indiana and Department of Pathology and Mary H. Weiser Food Allergy Center and Rogel Center for Cancer Research, University of Michigan School of Medicine, Ann Arbor, Michigan (C.H.K.).
Kyoung-Jae WonDepartment of Industrial and Molecular Pharmaceutics (H.L., X.Y., P.-R.J., K.-J.W., H.J.), Department of Pharmacy Practice (H.J.), and College of Pharmacy, and Department of Comparative Pathobiology, College of Veterinary Medicine (H.L.), Purdue University, West Lafayette, Indiana and Department of Pathology and Mary H. Weiser Food Allergy Center and Rogel Center for Cancer Research, University of Michigan School of Medicine, Ann Arbor, Michigan (C.H.K.).
Chang H KimDepartment of Industrial and Molecular Pharmaceutics (H.L., X.Y., P.-R.J., K.-J.W., H.J.), Department of Pharmacy Practice (H.J.), and College of Pharmacy, and Department of Comparative Pathobiology, College of Veterinary Medicine (H.L.), Purdue University, West Lafayette, Indiana and Department of Pathology and Mary H. Weiser Food Allergy Center and Rogel Center for Cancer Research, University of Michigan School of Medicine, Ann Arbor, Michigan (C.H.K.).
Hyunyoung JeongDepartment of Industrial and Molecular Pharmaceutics (H.L., X.Y., P.-R.J., K.-J.W., H.J.), Department of Pharmacy Practice (H.J.), and College of Pharmacy, and Department of Comparative Pathobiology, College of Veterinary Medicine (H.L.), Purdue University, West Lafayette, Indiana and Department of Pathology and Mary H. Weiser Food Allergy Center and Rogel Center for Cancer Research, University of Michigan School of Medicine, Ann Arbor, Michigan (C.H.K.) youngjeong@purdue.edu.ORCID 0000-0001-7769-7676
Purdue University West Lafayette · US

Funding

Homing of Functionally Distinct ILC SubsetsR01AI121302 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KIM, CHANG H · 2016 to 2020
$1.9M
Gut bacterial O-demethylationR21AT011565 · NCCIH · PURDUE UNIVERSITY · PI JEONG, HYUNYOUNG, LEE, HYUNWOO · 2021 to 2022
$438k
Pregnane X receptor (PXR)-activating gut bacterial metabolitesR21AT011391 · NCCIH · PURDUE UNIVERSITY · PI JEONG, HYUNYOUNG, LEE, HYUNWOO · 2022 to 2023
$425k
Mobilization and trafficking of central ILC progenitorsR56AI173179 · NIAID · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KIM, CHANG H · 2023 to 2023
$148k
NCCIH NIH HHS R21 AT011391NCCIH NIH HHS R21 AT011565NIAID NIH HHS R01 AI121302NIAID NIH HHS R56 AI173179
6 · The paper itself

Abstract

The mammalian gut microbiota plays diverse and essential roles in modulating host physiology. Key mediators determining the outcome of the microbiota-host interactions are the small molecule metabolites produced by the gut microbiota. The liver is a major organ exposed to gut microbial metabolites, and it serves as the nexus for maintaining healthy interactions between the gut microbiota and the host. At the same time, the liver is the primary target of potentially harmful gut microbial metabolites. In this review, we provide an up-to-date list of gut microbial metabolites that have been identified to either increase or decrease host susceptibility to acetaminophen (APAP)-induced liver injury. The signaling pathways and molecular factors involved in the progression of APAP-induced hepatotoxicity are well-established, and we propose that the mouse model of APAP-induced hepatotoxicity serves as a model system for uncovering gut microbial metabolites with previously unknown functions. Furthermore, we envision that gut microbial metabolites identified to alter APAP-induced hepatotoxicity likely have broader implications in other liver diseases. SIGNIFICANCE STATEMENT: This review provides an overview of the role of the gut microbiota in modulating the host susceptibility to acetaminophen (APAP)-induced liver injury. It focuses on the roles of gut bacterial small molecule metabolites as mediators of the interaction between the gut microbiota and the liver. It also illustrates the utility of APAP-induced liver injury as a model to identify gut microbial metabolites with biological function.

Indexed as

AcetaminophenChemical and Drug Induced Liver InjuryGastrointestinal MicrobiomeAnalgesics, Non-NarcoticAnimalsDisease SusceptibilityHumansLiverMiceAcetaminophenAnalgesics, Non-Narcotic

Identifiers

PMID38302428
PMCPMC11257691
OpenAlexW4391428416

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.