Evidence map›Paper›PMID 34026559›Full record

ReviewToxicology reports2021

Drug-induced-acute liver failure: A critical appraisal of the thioacetamide model for the study of hepatic encephalopathy.

Ali Sepehrinezhad, Ali Shahbazi, Sajad Sahab Negah, Mohammad Taghi Joghataei, Fin Stolze Larsen

Open access · goldAbstract readReview
In one paragraph

Review in Toxicology reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 59 citations in OpenAlex.

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  5. Improvement effect of Biluochun tea active extract on CClFood science and biotechnology · 2025
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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

5 authors at 3 institutions in 2 countries.

Ali SepehrinezhadDepartment of Neuroscience, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran.
Ali ShahbaziCellular and Molecular Research Center, Iran University of Medical Sciences, Tehran, Iran.
Sajad Sahab NegahNeuroscience Research Center, Mashhad University of Medical Sciences, Mashhad, Iran.
Mohammad Taghi JoghataeiDepartment of Neuroscience, Faculty of Advanced Technologies in Medicine, Iran University of Medical Sciences, Tehran, Iran.
Fin Stolze LarsenDepartment of Hepatology CA-3163, Rigshospitalet, Copenhagen University Hospital, Blegdamsvej 9, 2100, Copenhagen, Denmark.
Iran University of Medical Sciences · IRCopenhagen University Hospital · DKMashhad University of Medical Sciences · IR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hepatic encephalopathy (HE) following acute and chronic liver failure is defined as a complex of neuropsychiatric abnormalities, such as discrete personal changes, sleep disorder, forgetfulness, confusion, and decreasing the level of consciousness to coma. The use and design of suitable animal models that represent clinical features and pathological changes of HE are valuable to map the molecular mechanisms that result in HE. Among different types of animal models, thioacetamide (TAA) has been used extensively for the induction of acute liver injury and HE. This agent is not directly hepatotoxic but its metabolites induce liver injury through the induction of oxidative stress and produce systemic inflammation similar to that seen in acute HE patients. In this short review article, we shortly review the most important pathological findings in animal models of acute HE following the administration of TAA.

Indexed as

Acute liver failureALT, alanine aminotransferaseAnimal modelAQP4, aquaporin 4 water channelAST, aspartate aminotransferaseB7, B7 molecules (CD80+CD86)BBB, blood-brain barrierCBF, cerebral blood flowCCL2, chemokine ligand 2CNS, central nervous systemCTLA4, Cytotoxic T-lymphocyte-associated Protein 4CYP2E1, Cytochrome P450 family 2 subfamily E member 1GFAP, glial fibrillary acidic proteinHE, hepatic encephalopathyHepatic encephalopathyIba1, ionized calcium-binding adaptor molecule 1IL-6, interleukin 6IL-β, interleukin 1 βJNK, c-Jun N-terminal kinaseNAC, N-acetylcysteineNF-κB, nuclear factor κBOA, L-ornithine-l-aspartateROS, reactive oxygen speciesTAA, thioacetamideTASO2, thioacetamide sulfdioxideTASO, thioacetamide sulfoxideThioacetamideTLR-2, toll-like receptor 2TLR-4, toll-like receptor 4TNFα, tumor necrosis factor αToxicity pathway

Identifiers

PMID34026559
PMCPMC8122178
OpenAlexW3163903160

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.