ReviewMetabolic brain disease2009
Signaling factors in the mechanism of ammonia neurotoxicity.
Review in Metabolic brain disease, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
What it found
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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
62 citing papers in PubMed, 132 citations in OpenAlex.
- Differential metabolic and cellular brain regional susceptibility in adult rats with chronic liver disease.Metabolic brain disease · 2026Article
- Mechanism of Ammonia-Induced Brain Damage in Chinese Striped-Necked Turtle (Mauremys sinensis).Integrative zoology · 2026Article
- Littorina snails and Microphallus trematodes: Diverse consequences of the trematode-induced metabolic shifts.Parasitology research · 2024Article
- Multi-algorithm cooperation research of WRKY genes under nitrogen stress in Panax notoginseng.Protoplasma · 2023Article
- Branched chain amino acids in hepatic encephalopathy and sarcopenia in liver cirrhosis: Evidence and uncertainties.World journal of gastroenterology · 2023Review
- Effect of berrycactus fruit (Open life sciences · 2023Article
- Hyperammonemia in Inherited Metabolic Diseases.Cellular and molecular neurobiology · 2022Review
- Impact of L-ornithine L-aspartate on non-alcoholic steatohepatitis-associated hyperammonemia and muscle alterations.Frontiers in nutrition · 2022Article
- A Sarcina bacterium linked to lethal disease in sanctuary chimpanzees in Sierra Leone.Nature communications · 2021Article
- The Role of Amino Acids in Neurotransmission and Fluorescent Tools for Their Detection.International journal of molecular sciences · 2020Review
- N-acetyl cysteine treatment preserves mitochondrial indices of functionality in the brain of hyperammonemic mice.Clinical and experimental hepatology · 2020Article
- Article
- Ammonia-induced mitochondrial impairment is intensified by manganese co-exposure: relevance to the management of subclinical hepatic encephalopathy and cirrhosis-associated brain injury.Clinical and experimental hepatology · 2019Article
- Protective mechanism of testosterone on cognitive impairment in a rat model of Alzheimer's disease.Neural regeneration research · 2019Article
- Article
- The role of Branched Chain Amino Acids in the treatment of hepatic Encephalopathy.Journal of clinical and experimental hepatology · 2018Review
- Hyperammonemia in Hepatic Encephalopathy.Journal of clinical and experimental hepatology · 2018Review
- Ammonia-induced mitochondrial dysfunction and energy metabolism disturbances in isolated brain and liver mitochondria, and the effect of taurine administration: relevance to hepatic encephalopathy treatment.Clinical and experimental hepatology · 2017Article
- Genistein inhibited ammonia induced astrocyte swelling by inhibiting NF-κB activation-mediated nitric oxide formation.Metabolic brain disease · 2017Article
- Ammonia toxicity: from head to toe?Metabolic brain disease · 2017Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Mechanisms involved in hepatic encephalopathy (HE) still remain poorly understood. It is generally accepted that ammonia plays a major role in this disorder, and that astrocytes represent the principal target of ammonia neurotoxicity. In recent years, studies from several laboratories have uncovered a number of factors and pathways that appear to be critically involved in the pathogenesis of this disorder. Foremost is oxidative and nitrosative stress (ONS), which is largely initiated by an ammonia-induced increase in intracellular Ca(2+). Such increase in Ca(2+) activates a number of enzymes that promote the synthesis of reactive oxygen-nitrogen species, including constitutive nitric oxide synthase, NADPH oxidase and phospholipase A2. ONS subsequently induces the mitochondrial permeability transition, and activates mitogen-activated protein kinases and the transcription factor, nuclear factor-kappaB (NF-kappaB). These factors act to generate additional reactive oxygen-nitrogen species, to phosphorylate various proteins and transcription factors, and to cause mitochondrial dysfunction. This article reviews the role of these factors in the mechanism of HE and ammonia toxicity with a focus on astrocyte swelling and glutamate uptake, which are important consequences of ammonia neurotoxicity. These pathways and factors provide attractive targets for identifying agents potentially useful in the therapy of HE and other hyperammonemic disorders.
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What OpenQuestion holds
Registered trials
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.