ArticleMolecular therapy. Nucleic acids2017
Identification of Novel Fibrosis Modifiers by In Vivo siRNA Silencing.
Article in Molecular therapy. Nucleic acids, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 43 citations in OpenAlex.
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- A thioacrylamide-based compound directly counteracts hepatic fibrosis with profound anti-obesity action.JHEP reports : innovation in hepatology · 2026Article
- FKBP10 as a prognostic biomarker and therapeutic target in hepatocellular carcinoma.Discover oncology · 2026Article
- Knockdown of Hyaluronan synthase 2 suppresses liver fibrosis in mice via induction of transcriptomic changes similar to 4MU treatment.Scientific reports · 2024Article
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- Metabolic crosstalk between skeletal muscle cells and liver through IRF4-FSTL1 in nonalcoholic steatohepatitis.Nature communications · 2023Article
- Role of follistatin-like protein 1 in liver diseases.Experimental biology and medicine (Maywood, N.J.) · 2023Review
- Experimental Workflow for Preclinical Studies of Human Antifibrotic Therapies.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Endogenous Follistatin-like 1 guarantees the immunomodulatory properties of mesenchymal stem cells during liver fibrotic therapy.Stem cell research & therapy · 2022Article
- Follistatin-like protein 1 and chronic liver disease progression: a novel pro-inflammatory and pro-fibrogenic mediator?Annals of translational medicine · 2022Article
- Susceptibility to kidney fibrosis in mice is associated with early growth response-2 protein and tissue inhibitor of metalloproteinase-1 expression.Kidney international · 2022Article
- Elevated Alpha 1(I) to Alpha 2(I) Collagen Ratio in Dermal Fibroblasts Possibly Contributes to Fibrosis in Systemic Sclerosis.International journal of molecular sciences · 2022Article
- RNA sequencing of LX-2 cells treated with TGF-β1 identifies genes associated with hepatic stellate cell activation.Molecular biology reports · 2021Article
- Identification of pathological transcription in autosomal dominant polycystic kidney disease epithelia.Scientific reports · 2021Article
- Targeting Follistatin like 1 ameliorates liver fibrosis induced by carbon tetrachloride through TGF-β1-miR29a in mice.Cell communication and signaling : CCS · 2020Article
- Emerging Roles of Matricellular Proteins in Systemic Sclerosis.International journal of molecular sciences · 2020Review
- FKBP10 Acts as a New Biomarker for Prognosis and Lymph Node Metastasis of Gastric Cancer by Bioinformatics Analysis and in Vitro Experiments.OncoTargets and therapy · 2020Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 2 countries.
Funding
Abstract
Fibrotic diseases contribute to 45% of deaths in the industrialized world, and therefore a better understanding of the pathophysiological mechanisms underlying tissue fibrosis is sorely needed. We aimed to identify novel modifiers of tissue fibrosis expressed by myofibroblasts and their progenitors in their disease microenvironment through RNA silencing in vivo. We leveraged novel biology, targeting genes upregulated during liver and kidney fibrosis in this cell lineage, and employed small interfering RNA (siRNA)-formulated lipid nanoparticles technology to silence these genes in carbon-tetrachloride-induced liver fibrosis in mice. We identified five genes, Egr2, Atp1a2, Fkbp10, Fstl1, and Has2, which modified fibrogenesis based on their silencing, resulting in reduced Col1a1 mRNA levels and collagen accumulation in the liver. These genes fell into different groups based on the effects of their silencing on a transcriptional mini-array and histological outcomes. Silencing of Egr2 had the broadest effects in vivo and also reduced fibrogenic gene expression in a human fibroblast cell line. Prior to our study, Egr2, Atp1a2, and Fkbp10 had not been functionally validated in fibrosis in vivo. Thus, our results provide a major advance over the existing knowledge of fibrogenic pathways. Our study is the first example of a targeted siRNA assay to identify novel fibrosis modifiers in vivo.
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Registered trials
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