ArticleThe Journal of biological chemistry2021
A retinoic acid receptor β2 agonist attenuates transcriptome and metabolome changes underlying nonalcohol-associated fatty liver disease.
Article in The Journal of biological chemistry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- MicroRNA-34a Promotes Hepatic Lipid Accumulation Through RXRα Suppression and Is Reversed by 9-International journal of molecular sciences · 2026Article
- Key Early Changes in Oral Squamous Cell Carcinogenesis Are Accelerated by Ectopic BMI1 Expression.Cancer research communications · 2026Article
- The Vicious Circle of Metabolic Dysfunction-Associated Steatotic Liver Disease When Micronutrient Deficiency Drives Microbial Imbalance and Liver Injury.Life (Basel, Switzerland) · 2025Review
- USP25 directly interacts with and deubiquitinates PPARα to increase PPARα stability in hepatocytes and attenuate high-fat diet-induced MASLD in mice.Cell death and differentiation · 2025Article
- Exogenous BMI1 expression aggravates oral squamous cell carcinomas in tongue epithelia.Neoplasia (New York, N.Y.) · 2025Article
- Ethanol causes rapid decreases in the hepatic retinoid levels shaping the early steps of alcohol-associated liver disease.Alcohol, clinical & experimental research · 2025Article
- Retinoic acid receptor-β deletion in a model of early pancreatic ductal adenocarcinoma (PDAC) tumorigenesis.American journal of cancer research · 2025Article
- The transcription factor BMI1 increases hypoxic signaling in oral cavity epithelia.Biochimica et biophysica acta. Molecular basis of disease · 2024Article
- Examining the Pathogenesis of MAFLD and the Medicinal Properties of Natural Products from a Metabolic Perspective.Metabolites · 2024Review
- Targeting nuclear receptors for NASH/MASH: From bench to bedside.Liver research (Beijing, China) · 2024Article
- Retinoic acid receptor α activity in proximal tubules prevents kidney injury and fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Exploring the interactions between metabolic dysfunction-associated fatty liver disease and micronutrients: from molecular mechanisms to clinical applications.Frontiers in nutrition · 2024Review
- The roles of nuclear receptors in cholesterol metabolism and reverse cholesterol transport in nonalcoholic fatty liver disease.Hepatology communications · 2024Review
- Retinoic Acid Signaling in Fatty Liver Disease.Liver research (Beijing, China) · 2023Article
- Retinoic Acid Receptor β Loss in Hepatocytes Increases Steatosis and Elevates the Integrated Stress Response in Alcohol-Associated Liver Disease.International journal of molecular sciences · 2023Article
- Fibrogenic Pathways in Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD).International journal of molecular sciences · 2022Review
- Article
- Retinoids in the Pathogenesis and Treatment of Liver Diseases.Nutrients · 2022Review
- Tormentic Acid Ameliorates Hepatic FibrosisFrontiers in pharmacology · 2022Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Nonalcohol-associated fatty liver disease (NAFLD) is characterized by excessive hepatic accumulation of fat that can progress to steatohepatitis, and currently, therapeutic options are limited. Using a high-fat diet (HFD) mouse model of NAFLD, we determined the effects of the synthetic retinoid, AC261066, a selective retinoic acid receptor β2 (RARβ2) agonist, on the global liver transcriptomes and metabolomes of mice with dietary-induced obesity (DIO) using genome-wide RNA-seq and untargeted metabolomics. We found that AC261066 limits mRNA increases in several presumptive NAFLD driver genes, including Pklr, Fasn, Thrsp, and Chchd6. Importantly, AC261066 limits the increases in the transcript and protein levels of KHK, a key enzyme for fructose metabolism, and causes multiple changes in liver metabolites involved in fructose metabolism. In addition, in cultured murine hepatocytes, where exposure to fructose and palmitate results in a profound increase in lipid accumulation, AC261066 limits this lipid accumulation. Importantly, we demonstrate that in a human hepatocyte cell line, RARβ is required for the inhibitory effects of AC261066 on palmitate-induced lipid accumulation. Finally, our data indicate that AC261066 inhibits molecular events underpinning fibrosis and exhibits anti-inflammatory effects. In conclusion, changes in the transcriptome and metabolome indicate that AC261066 affects molecular changes underlying multiple aspects of NAFLD, including steatosis and fibrosis. Therefore, we suggest that AC261066 may have potential as an effective therapy for NAFLD.
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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.