ArticleInternational journal of molecular sciences2019
MicroRNA-29a Disrupts DNMT3b to Ameliorate Diet-Induced Non-Alcoholic Steatohepatitis in Mice.
Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 53 citations in OpenAlex.
- A novel C/EBPα-miR-335-5p-PRKAA2 regulatory axis drives hepatic lipid accumulation in MASLD.Scientific reports · 2026Article
- miR-29a-3p and TGF-β Axis in Fanconi anemia: mechanisms driving metabolic dysfunction and genome stability.Cellular and molecular life sciences : CMLS · 2025Article
- Role of micrornas in the pathophysiology and diagnosis of metabolic dysfunction-associated steatotic liver disease: A bibliometric review.Hepatology forum · 2025Review
- Down-regulation of miR-29 improves lipid metabolism in fatty liver of dairy cows.Animal biotechnology · 2024Article
- Research on the function of epigenetic regulation in the inflammation of non-alcoholic fatty liver disease.Life medicine · 2024Review
- MicroRNAs and Nonalcoholic Steatohepatitis: A Review.International journal of molecular sciences · 2023Review
- Interplays of liver fibrosis-associated microRNAs: Molecular mechanisms and implications in diagnosis and therapy.Genes & diseases · 2023Review
- MicroRNA-29a Mitigates Laminectomy-Induced Spinal Epidural Fibrosis and Gait Dysregulation by Repressing TGF-β1 and IL-6.International journal of molecular sciences · 2023Article
- Oxidative Stress Modulation by ncRNAs and Their Emerging Role as Therapeutic Targets in Atherosclerosis and Non-Alcoholic Fatty Liver Disease.Antioxidants (Basel, Switzerland) · 2023Review
- MiR-552-3p Regulates Multiple Fibrotic and Inflammatory genes Concurrently in Hepatic Stellate Cells Improving NASH-associated Phenotypes.International journal of biological sciences · 2023Article
- Theabrownin ameliorates liver inflammation, oxidative stress, and fibrosis in MCD diet-fed C57BL/6J mice.Frontiers in endocrinology · 2023Article
- Epidemiologic, Genetic, Pathogenic, Metabolic, Epigenetic Aspects Involved in NASH-HCC: Current Therapeutic Strategies.Cancers · 2022Review
- Noncoding RNAs as additional mediators of epigenetic regulation in nonalcoholic fatty liver disease.World journal of gastroenterology · 2022Review
- MiR-29a Curbs Hepatocellular Carcinoma Incidence via Targeting ofInternational journal of molecular sciences · 2022Article
- Heat Shock Protein 60 Restricts Release of Mitochondrial dsRNA to Suppress Hepatic Inflammation and Ameliorate Non-Alcoholic Fatty Liver Disease in Mice.International journal of molecular sciences · 2022Article
- Physiological Role of Bile Acids Modified by the Gut Microbiome.Microorganisms · 2021Review
- Ability of a Combined FIB4/miRNA181a Score to Predict Significant Liver Fibrosis in NAFLD Patients.Biomedicines · 2021Article
- Metabolic Consequences of Gestational Cannabinoid Exposure.International journal of molecular sciences · 2021Review
- MicroRNA-29a in Osteoblasts Represses High-Fat Diet-Mediated Osteoporosis and Body Adiposis through Targeting Leptin.International journal of molecular sciences · 2021Article
- Diagnosis and Therapeutic Management of Liver Fibrosis by MicroRNA.International journal of molecular sciences · 2021Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
MicroRNA-29 (miR-29) has been found to reduce liver inflammation and fibrosis following a liver injury. Meanwhile, DNA methyltransferase has been reported to participate in the development of non-alcoholic steatohepatitis (NASH). The aim of this study is to investigate the miR-29a regulation of methyltransferase signaling and epigenetic program in NASH progression. Methods: miR-29a transgenic mice (miR-29aTg mice) and wild-type littermates were subjected to the methionine-choline-deficient (MCD) diet-induced animal model of NASH. Primary hepatic stellate cells were transfected with a miR-29a mimic and antisense inhibitor. We then analyzed gene expressions with qRT-PCR, immunohistochemical stain, Western blot, and luciferase reporter assay. The results demonstrated that increased miR-29a alleviated the MCD diet-induced body weight loss and steatosis and decreased aspartate aminotransferase (AST) levels in mice. Furthermore, hepatic tissue in miR-29aTg mice displayed a weak fibrotic matrix, as shown with Sirius Red staining concomitant with low fibrotic α-SMA expression within affected tissues compared to the wild-type mice fed the MCD diet. Forced miR-29a expression reduced the MCD diet exaggeration of reactive oxygen species (ROS) production by immunohistochemically staining 8-OHdG. Increased miR-29a signaling also resulted in the downregulation of DNMT3b, TGF-β, IL-6, heme oxygenase-1 (HO-1), p-SMAD3, PI3K, and L3BII expression within the liver tissue. An in vitro luciferase reporter assay further confirmed that miR-29a mimic transfection reduced DNMT3b expression in primary HSCs. Our data provide new insights that miR-29a improves MCD diet-induced liver inflammation, steatosis and fibrosis, and highlight the potential of miR-29a targeted therapy for treating NASH.
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Registered trials
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