ArticleInternational journal of molecular sciences2023
Resmetirom Ameliorates NASH-Model Mice by Suppressing STAT3 and NF-κB Signaling Pathways in an RGS5-Dependent Manner.
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 31 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 48 citations in OpenAlex.
- Pooled it
- An antisense oligonucleotide targeting STK25 as a long-acting therapeutic candidate for early MASLD.Molecular therapy. Nucleic acids · 2026Article
- Repurposing Resmetirom to Suppress MASLD/MASH-HCC in the Dysmetabolic Era.Oncology and therapy · 2026Review
- Review
- Review
- Beta 2 adrenergic receptor agonists as a treatment for metabolic dysfunction-associated steatohepatitis (MASH).npj metabolic health and disease · 2026Article
- Therapeutic potential of TMSC-Exo for non-alcoholic fatty liver disease using the liver-on-a-chip model.Journal of translational internal medicine · 2026Article
- A microphysiological model of human MASLD reveals paradoxical response to resmetirom.Communications biology · 2026Article
- Design, Synthesis, and Anti-Hepatic Fibrosis Evaluation of Cordycepin Derivatives.Molecules (Basel, Switzerland) · 2026Article
- The Role of Kupffer Cells and Liver Macrophages in the Pathogenesis of Metabolic Dysfunction-Associated Steatotic Liver Disease.Biomedicines · 2026Review
- Evaluation of the Immortalized Primary Human Hepatocyte Cell Line Fa2N-4 as a Model for Metabolic Dysfunction-Associated Steatotic Liver Disease.Gastro hep advances · 2026Article
- An updated overview of alkaloids for the prevention and treatment of metabolic dysfunction-associated steatotic liver disease.Frontiers in pharmacology · 2026Review
- Differences between therapeutic mechanisms of resmetirom and semaglutide against MASH in western diet-fed MC4R-knockout mice.Scientific reports · 2025Article
- Mechanistic insights into post-translational modifications in hepatic fibrosis: pathogenic roles and therapeutic potentials.Journal of translational medicine · 2025Review
- Unlocking the potential of THR-β agonist therapies: resmetirom's chemistry, biology, and patent insights.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Inflammation in MASLD progression and cancer.JHEP reports : innovation in hepatology · 2025Review
- Lipid Hormones at the Intersection of Metabolic Imbalances and Endocrine Disorders.Current issues in molecular biology · 2025Review
- Macrophage Signaling Pathways in Health and Disease: From Bench to Bedside Applications.MedComm · 2025Review
- Integrated liver-secreted and plasma proteomics identify a predictive model that stratifies MASH.Cell reports. Medicine · 2025Article
- Resmetirom and thyroid hormone receptor-targeted treatment for metabolic dysfunction-associated steatotic liver disease (MASLD).Portal hypertension & cirrhosis · 2025Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Resmetirom, a liver-directed, orally active agonist of THR-β, could play a favorable role in treating NASH, but little is known about the underlying mechanism. A NASH cell model was established to test the preventive effect of resmetirom on this disease in vitro. RNA-seq was used for screening, and rescue experiments were performed to validate the target gene of the drug. A NASH mouse model was used to further elucidate the role and the underlying mechanism of resmetirom. Resmetirom effectively eliminated lipid accumulation and decreased triglyceride (TG) levels. In addition, repressed RGS5 in the NASH model could be recovered by resmetirom treatment. The silencing of RGS5 effectively impaired the role of resmetirom. In the NASH mouse model, obvious gray hepatization, liver fibrosis and inflammation, and increased macrophage infiltration were observed in liver tissues, while resmetirom almost returned them to normal conditions as observed in the control group. Pathological experimental data also confirmed that resmetirom has great potential in NASH treatment. Finally, RGS5 expression was suppressed in the NASH mouse model, but it was upregulated by resmetirom treatment, while the STAT3 and NF-κB signaling pathways were activated in NASH but inhibited by the agent. Resmetirom could improve NASH by recovering RGS5 expression and subsequently inactivating the STAT3 and NF-κB signaling pathways.
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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.