ArticleCell death & disease2017
MiR-130a-3p attenuates activation and induces apoptosis of hepatic stellate cells in nonalcoholic fibrosing steatohepatitis by directly targeting TGFBR1 and TGFBR2.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.
- 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
- Review
- Non-coding RNA networks in metabolic dysfunction-associated steatotic liver disease: Mechanisms and therapeutic perspectives.Liver research (Beijing, China) · 2026Review
- miR-130a-3p promotes fiber type transition and improves exercise tolerance in mice.Biological research · 2025Article
- miR-145-enriched BMSCs-derived exosomes ameliorate neurogenic erectile dysfunction in aged rats via TGFBR2 inhibition.Regenerative therapy · 2025Article
- Exploring the Putative Involvement of MALAT1 in Mediating the Beneficial Effect of Exendin-4 on Oleic Acid-Induced Lipid Accumulation in HepG2 Cells.Biomedicines · 2025Article
- Identifying novel therapeutic targets for non-alcoholic fatty liver disease using bioinformatics approaches: from drug repositioning to traditional Chinese medicine.Frontiers in bioinformatics · 2025Article
- MicroRNA: A Novel Class of Potential Biomarkers and Therapeutic Target for Non-Alcoholic Fatty Liver Disease/Nonalcoholic Steatohepatitis.MicroRNA (Shariqah, United Arab Emirates) · 2025Review
- Construction of a HSC activation-related lncRNA-miRNA-mRNA ceRNA regulatory network reveals potential molecules involved in liver fibrosis.Frontiers in genetics · 2025Article
- GMP-compliant, serum-free cultures preserve therapeutic potential of extracellular vesicles from human mesenchymal stromal cells.Frontiers in cell and developmental biology · 2025Article
- Proprotein convertase subtilisin/kexin 9 inhibitor downregulates microRNA-130a-3p expression in hepatocytes to alleviates atherosclerosis progression.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Linking fatty liver diseases to hepatocellular carcinoma by hepatic stellate cells.Journal of the National Cancer Center · 2024Review
- Two sides of the same coin: Non-alcoholic fatty liver disease and atherosclerosis.Vascular pharmacology · 2024Review
- Article
- Cellular heterogeneity and plasticity during NAFLD progression.Frontiers in molecular biosciences · 2023Review
- Review
- Targeted deletion of TGFβ1 in basal keratinocytes causes profound defects in stratified squamous epithelia and aberrant melanocyte migration.Developmental biology · 2022Article
- Resveratrol ameliorates nutritional steatohepatitis through the mmu‑miR‑599/PXR pathway.International journal of molecular medicine · 2022Article
- Pattern recognition receptor signaling and innate immune responses to schistosome infection.Frontiers in cellular and infection microbiology · 2022Review
- LncRNA MALAT1 Promotes PPARα/CD36-Mediated Hepatic Lipogenesis in Nonalcoholic Fatty Liver Disease by Modulating miR-206/ARNT Axis.Frontiers in bioengineering and biotechnology · 2022Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nonalcoholic fibrosing steatohepatitis is a uniform process that occurs throughout nonalcoholic fatty liver disease (NAFLD). MicroRNAs (miRNAs) have been shown to be involved in the biological processes, but the role and molecular mechanism of miRNAs in NAFLD are not entirely clear. In this study, we observed a significant reduction in the expression of miR-130a-3p in livers of a mouse model with fibrosis induced by a methionine-choline-deficient diet, of NAFLD patients, and in activated hepatic stellate cells (HSCs). A dual-luciferase activity assay confirmed that transforming growth factor-beta receptors (TGFBRs) 1 and 2 were both the target genes of miR-130a-3p. The hepatic expression of TGFBR1 and TGFBR2 was significantly increased. Moreover, the overexpression of miR-130a-3p in HSCs inhibited HSC activation and proliferation, concomitant with the decreased expression of TGFBR1, TGFBR2, Smad2, Smad3, matrix metalloproteinase-2 (MMP-2), MMP-9, type I collagen (Col-1), and Col-4. In addition, the overexpression of miR-130a-3p promoted HSC apoptosis by inducing the expression of caspase-dependent apoptosis genes. Transfection with si-TGFBR1 and si-TGFBR2 revealed effects on HSC function that were consistent with those of miR-130a-3p. TGFBR1 and TGFBR2 rescued the miR-130a-3p-mediated reductions in the mRNA and protein expression levels of Smad2, Smad3, Col-1, and Col-4. In conclusion, our findings suggest that miR-130a-3p might play a critical role in negatively regulating HSC activation and proliferation in the progression of nonalcoholic fibrosing steatohepatitis by directly targeting TGFBR1 and TGFBR2 via the TGF-β/SMAD signaling pathway.
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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.