ArticlePloS one2015
Systemic Delivery of scAAV8-Encoded MiR-29a Ameliorates Hepatic Fibrosis in Carbon Tetrachloride-Treated Mice.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
22 citing papers in PubMed, 41 citations in OpenAlex.
- miRNA-29 regulates epidermal and mesenchymal functions in skin repair.FEBS letters · 2025Article
- Proangiogenic role of circRNA-007371 in liver fibrosis.Cell proliferation · 2023Article
- Emerging therapeutic potential of adeno-associated virus-mediated gene therapy in liver fibrosis.Molecular therapy. Methods & clinical development · 2022Review
- Serum-derived miR-574-5p-containing exosomes contribute to liver fibrosis by activating hepatic stellate cells.Molecular biology reports · 2022Article
- Emerging Therapies for Charcot-Marie-Tooth Inherited Neuropathies.International journal of molecular sciences · 2021Review
- Insights into role of microRNAs in cardiac development, cardiac diseases, and developing novel therapies.Iranian journal of basic medical sciences · 2020Review
- Review
- Downregulation of the human peripheral myelin protein 22 gene by miR-29a in cellular models of Charcot-Marie-Tooth disease.Gene therapy · 2019Article
- Liver X Receptor α-Induced Cannabinoid Receptor 2 Inhibits Ubiquitin-Specific Peptidase 4 Through miR-27b, Protecting Hepatocytes From TGF-β.Hepatology communications · 2019Article
- Calpain 9 as a therapeutic target in TGFβ-induced mesenchymal transition and fibrosis.Science translational medicine · 2019Article
- MicroRNA29a Reverts the Activated Hepatic Stellate Cells in the Regression of Hepatic Fibrosis through Regulation of ATPase H⁺ Transporting V1 Subunit C1.International journal of molecular sciences · 2019Article
- Tissue-specific effects of targeted mutation of Mir29b1 in rats.EBioMedicine · 2018Article
- Safety and Efficacy of AAV Retrograde Pancreatic Ductal Gene Delivery in Normal and Pancreatic Cancer Mice.Molecular therapy. Methods & clinical development · 2018Article
- A circulating microRNA signature as noninvasive diagnostic and prognostic biomarkers for nonalcoholic steatohepatitis.BMC genomics · 2018Article
- Review
- A General Overview on Non-coding RNA-Based Diagnostic and Therapeutic Approaches for Liver Diseases.Frontiers in pharmacology · 2018Review
- Role of the microRNA-29 family in fibrotic skin diseases.Biomedical reports · 2017Article
- MicroRNA-29 overexpression by adeno-associated virus suppresses fibrosis and restores muscle function in combination with micro-dystrophin.JCI insight · 2017Article
- The MicroRNA 29 Family Promotes Type II Cell Differentiation in Developing Lung.Molecular and cellular biology · 2016Article
- Hepatic Stellate Cells and microRNAs in Pathogenesis of Liver Fibrosis.Journal of clinical medicine · 2016Review
Corrections and comments
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Authors and funding
13 authors at 9 institutions in 1 country.
Funding
Abstract
Fibrosis refers to the accumulation of excess extracellular matrix (ECM) components and represents a key feature of many chronic inflammatory diseases. Unfortunately, no currently available treatments specifically target this important pathogenic mechanism. MicroRNAs (miRNAs) are short, non-coding RNAs that post-transcriptionally repress target gene expression and the development of miRNA-based therapeutics is being actively pursued for a diverse array of diseases. Because a single miRNA can target multiple genes, often within the same pathway, variations in the level of individual miRNAs can potently influence disease phenotypes. Members of the miR-29 family, which include miR-29a, miR-29b and miR-29c, are strong inhibitors of ECM synthesis and fibrosis-associated decreases in miR-29 have been reported in multiple organs. We observed downregulation of miR-29a/b/c in fibrotic livers of carbon tetrachloride (CCl4) treated mice as well as in isolated human hepatocytes exposed to the pro-fibrotic cytokine TGF-β. Importantly, we demonstrate that a single systemic injection of a miR-29a expressing adeno-associated virus (AAV) can prevent and even reverse histologic and biochemical evidence of fibrosis despite continued exposure to CCl4. The observed therapeutic benefits were associated with AAV transduction of hepatocytes but not hepatic stellate cells, which are the main ECM producing cells in fibroproliferative liver diseases. Our data therefore demonstrate that delivery of miR-29 to the hepatic parenchyma using a clinically relevant gene delivery platform protects injured livers against fibrosis and, given the consistent fibrosis-associated downregulation of miR-29, suggests AAV-miR-29 based therapies may be effective in treating a variety of fibroproliferative disorders.
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Registered trials
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.