ArticleInternational journal of molecular sciences2023
The Mechanism of Hepatic Encephalopathy Induced by Thioacetamide Based on Metabolomics and Proteomics: A Preliminary Study.
Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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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.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Liraglutide Attenuates Multiorgan Oxidative, Astroglial, and Mitochondrial Stress Responses in Thioacetamide-Induced Hepatic Encephalopathy.International journal of molecular sciences · 2026Article
- Combined proteomics and metabolomics analyses revealed molecular signatures associated with proliferative diabetic retinopathy.Scientific reports · 2026Article
- Novel insights into cyanobacterial (microcystins) neurotoxicity in rats: hepatic encephalopathy.Archives of toxicology · 2026Article
- Editorial of Topic Issue "Chromatography-Mass Spectrometry Analysis in Biomedical Research and Clinical Laboratory".Molecules (Basel, Switzerland) · 2026Article
- Perspectives of Quantitative GC-MS, LC-MS, and ICP-MS in the Clinical Medicine Science-The Role of Analytical Chemistry.Journal of clinical medicine · 2024Article
- Preliminary Exploration of the Protective Mechanism of Eugenol Against Acute Liver Injury Induced by Thioacetamide Based on Metabolomics.Molecules (Basel, Switzerland) · 2024Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hepatic encephalopathy (HE) is a central nervous system dysfunction syndrome caused by acute and chronic liver failure or various portal systemic shunt disorders. HE arises from metabolic disorder and excludes other known types of encephalopathy. HE is a major cause of death in people with liver disease. Early diagnosis and timely treatment are key to improving HE prognosis. Herein, we established a model of HE and performed metabolomics to identify 50 significantly differential metabolites between the HE group and control group. The main metabolic pathways associated with these differential metabolites were the purine metabolism, pyrimidine metabolism, aminoacyl tRNA biosynthesis, and glucose metabolism. Through proteomics analysis, we identified 226 significantly differential proteins (52 up-regulated and 174 down-regulated). The main (Kyoto Encyclopedia of Genes and Genomes) enrichment pathways were the
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Registered trials
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