ArticleDisease models & mechanisms2020
Ammonia inhibits energy metabolism in astrocytes in a rapid and glutamate dehydrogenase 2-dependent manner.
Article in Disease models & mechanisms, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 49 citations in OpenAlex.
- Revisiting gut microbiota-driven ammonia metabolism: from disease burden to physiological adaptation.Gut microbes · 2026Review
- Urea cycle dysregulation and arginine pathways in the pathogenesis of NAFLD and NASH (Review).International journal of molecular medicine · 2026Review
- SIRT4 positively regulates autophagy via ULK1, but independently of HDAC6 and OPA1.FEBS open bio · 2026Article
- Beyond Organ Boundaries: Molecular Mechanisms of Hepatic Encephalopathy and Parkinson's Disease from the Perspective of the Gut-Liver-Brain Axis.Research (Washington, D.C.) · 2026Review
- Ammonia in cancer: dual roles and therapeutic strategies.Cancer cell international · 2025Review
- Review
- Brain Functional Connectivity Significantly Improves After Surgical Eradication of Porto-Systemic Shunting in Pediatric Patients.Life (Basel, Switzerland) · 2025Article
- Unveiling ammonia-induced cell death: a new frontier in clear cell renal cell carcinoma prognosis.Frontiers in immunology · 2025Article
- The Role of Neuroinflammation in the Pathogenesis of Hepatic Encephalopathy.Journal of immunology research · 2025Review
- Ammonia-induced stress response in liver disease progression and hepatic encephalopathy.Nature reviews. Gastroenterology & hepatology · 2024Review
- Evolution of Glutamate Metabolism viaInternational journal of molecular sciences · 2024Review
- Gut-derived ammonia contributes to alcohol-related fatty liver development via facilitating ethanol metabolism and provoking ATF4-dependent de novo lipogenesis activation.Metabolism: clinical and experimental · 2024Article
- Biological characteristics and functions of a novel glutamate dehydrogenase from Trichinella spiralis.Parasite (Paris, France) · 2024Article
- Neuron-Astrocyte Interactions: A Human Perspective.Advances in neurobiology · 2024Review
- Ammonium chloride reduces excitatory synaptic transmission onto CA1 pyramidal neurons of mouse organotypic slice cultures.Frontiers in cellular neuroscience · 2024Article
- CoClFEBS open bio · 2023Article
- Cellular Pathogenesis of Hepatic Encephalopathy: An Update.Biomolecules · 2023Review
- New Insight Into Mechanisms of Hepatic Encephalopathy: An Integrative Analysis Approach to Identify Molecular Markers and Therapeutic Targets.Bioinformatics and biology insights · 2023Article
- House ammonia exposure causes alterations in microbiota, transcriptome, and metabolome of rabbits.Frontiers in microbiology · 2023Article
- Transcriptome Profile in the Mouse Brain of Hepatic Encephalopathy and Alzheimer's Disease.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Astrocyte dysfunction is a primary factor in hepatic encephalopathy (HE) impairing neuronal activity under hyperammonemia. In particular, the early events causing ammonia-induced toxicity to astrocytes are not well understood. Using established cellular HE models, we show that mitochondria rapidly undergo fragmentation in a reversible manner upon hyperammonemia. Further, in our analyses, within a timescale of minutes, mitochondrial respiration and glycolysis were hampered, which occurred in a pH-independent manner. Using metabolomics, an accumulation of glucose and numerous amino acids, including branched chain amino acids, was observed. Metabolomic tracking of
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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.