ArticleInternational journal of molecular medicine2019
The A3 adenosine receptor agonist, namodenoson, ameliorates non‑alcoholic steatohepatitis in mice.
Article in International journal of molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 39 citations in OpenAlex.
- Randomised clinical trial: A phase 2 double-blind study of namodenoson in non-alcoholic fatty liver disease and steatohepatitis.Alimentary pharmacology & therapeutics · 2021Trial
- A3 Adenosine Receptor Agonists as Multisystem Disease Modifiers: From Molecular Signaling to Clinical Translation.Biomolecules · 2026Review
- The anti-obesity effect of namodenoson, an A3 adenosine receptor agonist.International journal of obesity (2005) · 2026Article
- Navigating liver cancer with mouse models: a comprehensive overview of HCC experimental systems.Journal of liver cancer · 2025Article
- Adenosine receptor subtype modulators: Insight into molecular mechanisms and their therapeutic application.American journal of translational research · 2025Review
- Adenosine A2B receptor activation regulates the balance between T helper 17 cells and regulatory T cells, and inhibits regulatory T cells exhaustion in experimental autoimmune myositis.Journal of cachexia, sarcopenia and muscle · 2024Article
- Purinergic Signaling in Non-Parenchymal Liver Cells.International journal of molecular sciences · 2024Review
- 2-Substituted (N)-Methanocarba AACS pharmacology & translational science · 2024Article
- Cryo-EM structures of adenosine receptor ANature communications · 2024Article
- Namodenoson at the Crossroad of Metabolic Dysfunction-Associated Steatohepatitis and Hepatocellular Carcinoma.Biomedicines · 2024Review
- The different effects of four adenosine receptors in liver fibrosis.Frontiers in pharmacology · 2024Article
- Targeting the A3 adenosine receptor to treat hepatocellular carcinoma: anti-cancer and hepatoprotective effects.Purinergic signalling · 2023Review
- GPCRs and fibroblast heterogeneity in fibroblast-associated diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023Review
- Knockout of Purinergic P2YInternational journal of molecular sciences · 2023Article
- Characterization of Dual-Acting AACS pharmacology & translational science · 2022Article
- Selective AACS medicinal chemistry letters · 2022Article
- AEuropean journal of medicinal chemistry · 2022Article
- Diagnostic and therapeutic strategies for non-alcoholic fatty liver disease.Frontiers in pharmacology · 2022Review
- ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism.Frontiers in physiology · 2022Review
- Purinergic signaling in diabetes and metabolism.Biochemical pharmacology · 2021Review
Corrections and comments
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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
The Wnt/β‑catenin pathway confers a chain of molecular events in livers affected by non‑alcoholic steatohepatitis (NASH). Namodenoson, a selective agonist of the A3 adenosine receptor (A3AR), which is highly expressed in pathological liver cells, induces a robust anti‑inflammatory effect in the liver, mediated via the de‑regulation of the Wnt/β‑catenin pathway. Namodenoson also acts as a liver protective agent by inhibiting ischemia/reperfusion injury. Based on these unique characteristics, we investigated the anti‑NASH effect of Namodenoson in murine models of steatohepatitis and in the LX2 human hepatic stellate cell line (HSC). In the STAM model, Namodenoson significantly decreased the non‑alcoholic fatty liver disease (NAFLD) activity score, NAS, demonstrating anti‑inflammatory and anti‑steatotic effects. In the carbon tetrachloride (CCl4) model, Namodenoson reversed alanine aminotransferase (ALT) to normal values and significantly improved liver inflammation and fibrosis, as well as the adiponectin and leptin levels. Namodenoson de‑regulated the Wnt/β‑catenin pathway in the liver extracts of the CCl4 model mice and in the LX2 HSCs, manifested by a decrease in the expression of phosphoinositide 3‑kinase (PI3K), nuclear factor κ‑light‑chain‑enhancer of activated B cells (NF‑κB), β‑catenin, lymphoid enhancer‑binding factor 1 (Lef‑1) and cyclin D1, and an increase in the expression level of glycogen synthase kinase 3β (GSK‑3β). The fibrosis marker, α‑smooth muscle actin (α‑SMA) was also de‑regulated, supporting the anti‑fibrotic effect of Namodenoson. On the whole, the findings of this study demonstrate that Namodenoson exerts an anti‑NASH effect mediated via the de‑regulation of the PI3K/NF‑κB/Wnt/β‑catenin signaling pathway. Thus, targeting A3AR may prove to be a novel direction in the pharmacotherapy of NAFLD/NASH.
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