ArticleJournal of cellular and molecular medicine2020
Long non-coding RNA (lncRNA) H19 induces hepatic steatosis through activating MLXIPL and mTORC1 networks in hepatocytes.
Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 60 papers.
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Who cites it
60 citing papers in PubMed, 113 citations in OpenAlex.
- Non-coding RNA networks in metabolic dysfunction-associated steatotic liver disease: Mechanisms and therapeutic perspectives.Liver research (Beijing, China) · 2026Review
- LncRNA TUG1 promotes hepatic lipid accumulation by targeting the miR-29a-3p/SREBP-2/HMGCR axis in MAFLD.Functional & integrative genomics · 2026Article
- miRNAs, lncRNAs, circRNAs and piRNAs in Nonalcoholic Fatty Liver Disease: Past, Present and Future.International journal of molecular sciences · 2025Review
- Advances in the Regulation of Lipid Metabolism by Non-Coding RNAs.Animals : an open access journal from MDPI · 2025Review
- Lactate transporter MCT4 regulates the hub genes for lipid metabolism and inflammation to attenuate intracellular lipid accumulation in non-alcoholic fatty liver disease.Genes & diseases · 2025Article
- Review of roles of RNA-binding proteins on NAFLD and the related pharmaceutical measures.Biomolecules & biomedicine · 2025Review
- LncRNA H19 promoted alcohol-associated liver disease through dysregulation of alternative splicing and methionine metabolism.Hepatology (Baltimore, Md.) · 2025Article
- Identification of tryptophan metabolism-related biomarkers for nonalcoholic fatty liver disease through network analysis.Endocrine connections · 2025Article
- Long Non-Coding RNAs in Non-Alcoholic Fatty Liver Disease; Friends or Foes?Cell biochemistry and biophysics · 2025Review
- Hypercholesterolemia as a Causal Risk Factor for COPD: Biomarker Discovery and Therapeutic Implications From NHANES Data.International journal of chronic obstructive pulmonary disease · 2025Article
- Metabolic Derangement in Non-Alcoholic Fatty Liver Disease: Opportunities for Early Diagnostic and Prognostic Markers.Current molecular medicine · 2025Review
- Biofluid-Derived Exosomal LncRNAs: Their Potential in Obesity and Related Comorbidities.Biology · 2024Review
- Mechanistic role of long non-coding RNAs in the pathogenesis of metabolic dysfunction-associated steatotic liver disease and fibrosis.eGastroenterology · 2024Article
- Long Noncoding RNAs in Diet-Induced Metabolic Diseases.International journal of molecular sciences · 2024Review
- LncRNA HOTAIR accelerates free fatty acid-induced inflammatory response in HepG2 cells by recruiting SRSF1 to stabilize MLXIPL mRNA.Cytotechnology · 2024Article
- Adipose-derived mesenchymal stem cells (MSCs) are a superior cell source for bone tissue engineering.Bioactive materials · 2024Article
- Long non-coding RNA HOX transcript antisense intergenic RNA depletion protects against alcoholic hepatitis through the microRNA-148a-3p/sphingosine 1-phosphate receptor 1 axis.Cell and tissue research · 2023Article
- Article
- Recent insights into the pathogenesis and therapeutic targets of chronic liver diseases.eGastroenterology · 2023Article
- The role of long non-coding RNAs in carbohydrate and fat metabolism in the liver.Non-coding RNA research · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver plays an essential role in regulating lipid metabolism, and chronically disturbed hepatic metabolism may cause obesity and metabolic syndrome, which may lead to non-alcoholic fatty liver disease (NAFLD). Increasing evidence indicates long non-coding RNAs (lncRNAs) play an important role in energy metabolism. Here, we investigated the role of lncRNA H19 in hepatic lipid metabolism and its potential association with NAFLD. We found that H19 was up-regulated in oleic acid-induced steatosis and during the development of high-fat diet (HFD)-induced NAFLD. Exogenous overexpression of H19 in hepatocytes induced lipid accumulation and up-regulated the expression of numerous genes involved in lipid synthesis, storage and breakdown, while silencing endogenous H19 led to a decreased lipid accumulation in hepatocytes. Mechanistically, H19 was shown to promote hepatic steatosis by up-regulating lipogenic transcription factor MLXIPL. Silencing Mlxipl diminished H19-induced lipid accumulation in hepatocytes. Furthermore, H19-induced lipid accumulation was effectively inhibited by PI3K/mTOR inhibitor PF-04691502. Accordingly, H19 overexpression in hepatocytes up-regulated most components of the mTORC1 signalling axis, which were inhibited by silencing endogenous H19. In vivo hepatocyte implantation studies further confirm that H19 promoted hepatic steatosis by up-regulating both mTORC1 signalling axis and MLXIPL transcriptional network. Collectively, these findings strongly suggest that H19 may play an important role in regulating hepatic lipid metabolism and may serve as a potential therapeutic 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.