ArticleMolecular medicine (Cambridge, Mass.)2019
miR-122 promotes hepatic lipogenesis via inhibiting the LKB1/AMPK pathway by targeting Sirt1 in non-alcoholic fatty liver disease.
Article in Molecular medicine (Cambridge, Mass.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers, 3 of them syntheses that pooled it.
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Who cites it
168 citing papers in PubMed, 3 syntheses or guidelines pooled it, 260 citations in OpenAlex.
- Comprehensive evaluation of GLP-1 receptor agonists: an umbrella review of clinical outcomes across multiple diseases.Nature communications · 2026Pooled it
- Revealing VNN1: An Emerging and Promising Target for Inflammation and Redox Balance.Immunity, inflammation and disease · 2025Pooled it
- Therapeutic Effects of microRNAs on Nonalcoholic Fatty Liver Disease (NAFLD) and Nonalcoholic Steatohepatitis (NASH): A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2023Pooled it
- Circulating Levels of microRNA-122 and Hepatic Fat Change in Response to Weight-Loss Interventions: CENTRAL Trial.The Journal of clinical endocrinology and metabolism · 2022Trial
- Role of adipocytes and their derived extracellular vesicles in the progression, diagnosis and treatment of liver diseases (Review).International journal of molecular medicine · 2026Review
- MicroRNA-122 as a regulator and biomarker of liver disease.Journal of molecular medicine (Berlin, Germany) · 2026Review
- The LKB1-AMPK pathway in NAFLD: molecular mechanisms and therapeutic implications.Journal of physiology and biochemistry · 2026Review
- Extracellular Vesicle-Based miRNA Profiling in Metabolic Dysfunction-Associated Steatotic Liver Disease: A Secondary Analysis of the MULTISITE Clinical Trial.Journal of extracellular biology · 2026Article
- MicroRNA Crosstalk in Metabolic Disorders: The Dual Role of miR-122 and miR-34a in NAFLD and Type 2 Diabetes.Molecular biotechnology · 2026Review
- Sanzi Sijun Formula Alleviates Lipotoxic Liver Injury in Metabolic Dysfunction-Associated Steatotic Liver Disease via AMPK/SIRT1 Signaling Pathway.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Molecular Mechanisms Associated with Metabolic Dysfunction: Contributions of Nutritional Genomics.Metabolites · 2026Review
- Targeting the cytokine-epigenetic axis: a new paradigm and prospects for disease treatment.European cytokine network · 2026Review
- MicroRNA-SIRT1 crosstalk in liver diseases: molecular regulation of metabolism, inflammation, and cell survival.Molecular biology reports · 2026Review
- The role of hepatocyte epigenetics in the pathogenesis of metabolic dysfunction-associated steatotic liver disease.Communications medicine · 2026Review
- Mechanism of miR-140-3p reducing anesthesia induced neurotoxicity by downregulating BACE1 expression.Journal of neurovirology · 2026Article
- m1A Epitranscriptomic Control of NUPR1 by YTHDF1 Exacerbates Metabolic Dysregulation in Nonalcoholic Fatty Liver Disease.Journal of clinical and translational hepatology · 2026Article
- Deficiency of GCN5 exacerbates pulmonary fibrosis by disrupting the LKB1-AMPK pathway.Cell communication and signaling : CCS · 2026Article
- Deregulated miR-487b-3p in Patients with Non-Alcoholic Fatty Liver Disease and Its Regulatory Effect on Insulin Resistance.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2026Article
- Circulating MicroRNA Profiling for Phenotypic Stratification in Patients with Metabolic Dysfunction-Associated Fatty Liver Disease: A Candidate-Based Study.Current issues in molecular biology · 2026Article
- Predominant miRNAs in Animal-Source Foods and Bioinformatic Analysis.Current issues in molecular biology · 2026Article
108 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNon-alcoholic fatty liver disease (NAFLD) is a common hepatic disease with an increasing prevalence but an unclear aetiology. This study aimed to investigate the functional implications of microRNA-122 (miR-122) in the pathogenesis of NAFLD and the possible molecular mechanisms.
methodsBoth in vitro and in vivo models of NAFLD were generated by treating HepG2 and Huh-7 cells with free fatty acids (FFA) and by feeding mice a high-fat diet (HFD), respectively. HE and Oil Red O staining were used to examine liver tissue morphology and lipid deposition, respectively. Immunohistochemical (IHC) staining was used to examine Sirt1 expression in liver tissues. qRT-PCR and Western blotting were employed to measure the expression of miR-122, Sirt1, and proteins involved in lipogenesis and the AMPK pathway. Enzyme-linked immunosorbent assay (ELISA) was used to quantify triglyceride (TG) levels in HepG2 and Huh-7 cells and in liver tissues. The interaction between miR-122 and the Sirt1 gene was further examined by a dual luciferase reporter assay and RNA-immunoprecipitation (RIP).
resultsNAFLD hepatic tissues and FFA-treated HepG2 and Huh-7 cells presented excess lipid production and TG secretion, accompanied by miR-122 upregulation, Sirt1 downregulation, and potentiated lipogenesis-related genes. miR-122 suppressed Sirt1 expression via binding to its 3'-untranslated region (UTR). Knockdown of miR-122 effectively mitigated excessive lipid production and suppressed the expression of lipogenic genes in FFA-treated HepG2 and Huh-7 cells via upregulating Sirt1. Furthermore, miR-122 knockdown activated the LKB1/AMPK signalling pathway.
conclusionThe inhibition of miR-122 protects hepatocytes from lipid metabolic disorders such as NAFLD and suppresses lipogenesis via elevating Sirt1 and activating the AMPK pathway. These data support miR-122 as a promising biomarker and drug target 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.