ArticleMolecular therapy : the journal of the American Society of Gene Therapy2016
MiR-29a Assists in Preventing the Activation of Human Stellate Cells and Promotes Recovery From Liver Fibrosis in Mice.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers, 1 of them a synthesis that pooled it.
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Who cites it
54 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- Research trends of mitochondrial dysfunction in hepatic fibrosis: a bibliometric analysis.Frontiers in physiology · 2026Pooled it
- The Matrix Reloaded: The Hepatic Matrisome as a Therapeutic Opportunity to Fight Liver Fibrosis.Biomolecules · 2026Review
- Modulation of miRNA networks by exercise in muscular dystrophies: therapeutic insights and future directions.Molecular and cellular biochemistry · 2026Review
- The Small Molecule H89 Facilitates Mesenchymal Stem Cell-derived Extracellular Vesicle Release and Optimizes Therapeutic Efficacy in Liver Regeneration.Journal of extracellular vesicles · 2026Article
- Leveraging extracellular vesicle biology for novel tests and therapeutics for kidney fibrosis.Clinical and translational medicine · 2026Review
- <p>Beyond hepatic stellate cell heterogeneity: Resolving fibrosis, restoring regeneration (Review)</p>.International journal of molecular medicine · 2026Review
- Roles of Extracellular Vesicle-Derived microRNAs in Metabolic Dysfunction-Associated Steatotic Liver Disease to Hepatocellular Carcinoma.Biomedicines · 2026Review
- Unravelling the reversion mechanisms of activated hepatic stellate cell properties by extracellular vesicles from mesenchymal stem cells.World journal of stem cells · 2025Review
- Evaluation of Five Plasma miRNAs as Biomarkers for Minimally Invasive Staging of Liver Fibrosis in β-Thalassaemia Patients.International journal of molecular sciences · 2025Article
- Genomic medicine in hepatology: mechanisms and liver treatment strategies.Molecular medicine (Cambridge, Mass.) · 2025Review
- Hepatocyte delivery of miR-34b/c reduces hepatic stellate cell activation and improves liver fibrosis.Molecular therapy. Nucleic acids · 2025Article
- Caspase-9 activates β-catenin signaling to promote pulmonary fibrosis.Journal of translational medicine · 2025Article
- LNP-encapsulated miRNA29b for corneal repair: A novel approach to combat fibrosis.Materials today. Bio · 2025Article
- The potential of miR-29 in modulating tumor angiogenesis: a comprehensive review.Discover oncology · 2025Review
- Development of novel nucleic acid therapy aimed at directly controlling liver fibrosis.Molecular therapy. Nucleic acids · 2025Article
- An optimised faecal microRNA sequencing pipeline reveals fibrosis in Trichuris muris infection.Nature communications · 2025Article
- Fibroblast exosomes promote wound healing and improve the quality of healed skin via miR-29a-3p-mediated KEAP1/Nrf2 pathway activation.Burns & trauma · 2025Article
- Novel insights into the role of immunomodulatory extracellular vesicles in the pathogenesis of liver fibrosis.Biomarker research · 2024Review
- Early stress exposure on zebrafish development: effects on survival, malformations and molecular alterations.Fish physiology and biochemistry · 2024Article
- Serum miR‑29 is increased in mice with early liver fibrosis.Experimental and therapeutic medicine · 2024Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The microRNA-29 (miR-29) family is known to suppress the activation of hepatic stellate cells (HSCs) and reversibly control liver fibrosis; however, the mechanism of how miR-29a controls liver fibrosis remains largely unknown. This study was conducted to clarify the mechanism of anti-fibrotic effect of miR-29a and to explore if miR-29a is a promising candidate for nucleic acid medicine against liver fibrosis. Two liver fibrosis murine models (carbon tetrachloride or thioacetamide) were used. MiR-29a mixed with atelocollagen was systemically administered. Hepatic fibrosis was evaluated by histological analysis and the expression levels of fibrosis-related genes. We observed that miR-29a treatment dramatically accelerated the reversion of liver fibrosis in vivo. Additionally, miR-29a regulated the mRNA expression of collagen type I alpha 1 (COL1A1) and platelet-derived growth factor C (PDGFC). We also noted that miR-29a significantly suppressed COL1A1 mRNA expression and cell viability and significantly increased caspase-9 activity (P < 0.05) in LX-2 cells. Pretreatment of miR-29a inhibited activation of LX-2 cell by transforming growth factor beta treatment. MiR-29a exhibited anti-fibrotic effect without cell toxicity in vivo and directly suppressed the expression of PDGF-related genes as well as COL1A1 and induced apoptosis of LX-2 cells. MiR-29a is a promising nucleic acid inhibitor to target liver fibrosis.
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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.