ArticleGastroenterology2023
Hepatocyte Adenosine Kinase Promotes Excessive Fat Deposition and Liver Inflammation.
Article in Gastroenterology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- Quantitative Multifrequency Ultrasound Imaging Using Narrowband Pulsing for Tissue Characterization.Investigative radiology · 2026Article
- Neointimal hyperplasia and vascular restenosis: from molecular mechanisms to therapeutic interventions.Molecular biomedicine · 2026Review
- The role of hepatocyte epigenetics in the pathogenesis of metabolic dysfunction-associated steatotic liver disease.Communications medicine · 2026Review
- Inhibition of adenosine kinase alleviates hypertrophic cardiomyopathy by ameliorating coronary microvascular dysfunction.ESC heart failure · 2026Article
- Comparison and Characteristics of MASLD Mouse Models.Biomedicines · 2026Review
- Vitamin D and Metabolic Dysfunction-Associated Steatotic Liver Disease: Molecular Mechanisms and Clinical Implications-A Narrative Review.International journal of molecular sciences · 2026Review
- Effects of Betaine on DNA Methylation Level, Expression Level, and Fat Synthesis ofAnimals : an open access journal from MDPI · 2026Article
- PPARa-FSP1 axis modulates lipid peroxidation-induced neuronal ferroptosis to promote functional recovery in mouse model of traumatic spinal cord injury.Cellular and molecular life sciences : CMLS · 2026Article
- Adenosine metabolic clearance maintains liver homeostasis by licensing arginine methylation of RIPK1.The Journal of experimental medicine · 2026Article
- Modulation of Inflammation-Driven Hepatocarcinogenesis: The Hepatic Immune Microenvironment, Gut-Liver Axis, and Neuroregulation.Journal of hepatocellular carcinoma · 2026Review
- Genistein ameliorates non-alcoholic fatty liver disease in mice by modulating gut microbiota and hepatic macrophage polarization.Scientific reports · 2025Article
- Plasma proteins and onset of atherosclerosis: integrating human plasma proteogenomics, transcriptomics and in vivo evidence.Journal of translational medicine · 2025Article
- Immunopathogenic mechanisms and immunoregulatory therapies in MASLD.Cellular & molecular immunology · 2025Review
- Deciphering Age-Dependent ECM Remodelling in Liver: Proteomic Profiling and Its Implications for Aging and Therapeutic Targets.Cell proliferation · 2025Article
- Comparative study on the effects of high fat diet and capsicum diet on the digestive organs of guinea pigs.Scientific reports · 2025Article
- High sensitivity C-reactive protein implicates heterogeneous metabolic phenotypes and severity in metabolic dysfunction associated-steatotic liver disease.BMC gastroenterology · 2025Article
- Enpp1 ameliorates MAFLD by regulating hepatocyte lipid metabolism through the AMPK/PPARα signaling pathway.Cell & bioscience · 2025Article
- Role of genetic variants and DNA methylation of lipid metabolism-related genes in metabolic dysfunction-associated steatotic liver disease.Frontiers in physiology · 2025Review
- Identification of Potential Diagnostic Biomarkers and Drug Targets for Endometriosis from a Genetic Perspective: A Mendelian Randomization Study.Gynecologic and obstetric investigation · 2025Article
- HFD feeding for seven months abolishes STING disruption-driven but not female sex-based protection against hepatic steatosis and inflammation in mice.The Journal of nutritional biochemistry · 2025Article
Corrections and comments
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Authors and funding
18 authors at 6 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsNonalcoholic fatty liver disease is highly associated with obesity and progresses to nonalcoholic steatohepatitis when the liver develops overt inflammatory damage. While removing adenosine in the purine salvage pathway, adenosine kinase (ADK) regulates methylation reactions. We aimed to study whether hepatocyte ADK functions as an obesogenic gene/enzyme to promote excessive fat deposition and liver inflammation.
methodsLiver sections of human subjects were examined for ADK expression using immunohistochemistry. Mice with hepatocyte-specific ADK disruption or overexpression were examined for hepatic fat deposition and inflammation. Liver lipidomics, hepatocyte RNA sequencing (RNA-seq), and single-cell RNA-seq for liver nonparenchymal cells were performed to analyze ADK regulation of hepatocyte metabolic responses and hepatocyte-nonparenchymal cells crosstalk.
resultsWhereas patients with nonalcoholic fatty liver disease had increased hepatic ADK levels, mice with hepatocyte-specific ADK disruption displayed decreased hepatic fat deposition on a chow diet and were protected from diet-induced excessive hepatic fat deposition and inflammation. In contrast, mice with hepatocyte-specific ADK overexpression displayed increased body weight and adiposity and elevated degrees of hepatic steatosis and inflammation compared with control mice. RNA-seq and epigenetic analyses indicated that ADK increased hepatic DNA methylation and decreased hepatic Ppara expression and fatty acid oxidation. Lipidomic and single-cell RNA-seq analyses indicated that ADK-driven hepatocyte factors, due to mitochondrial dysfunction, enhanced macrophage proinflammatory activation in manners involving increased expression of stimulator of interferon genes.
conclusionsHepatocyte ADK functions to promote excessive fat deposition and liver inflammation through suppressing hepatocyte fatty acid oxidation and producing hepatocyte-derived proinflammatory mediators. Therefore, hepatocyte ADK is a therapeutic target for managing obesity and nonalcoholic fatty liver disease.
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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.