ArticleEMBO molecular medicine2015
Fusion protein of retinol-binding protein and albumin domain III reduces liver fibrosis.
Article in EMBO molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 32 citations in OpenAlex.
- Nanoparticle-based systems for liver therapy: Overcoming fibrosis and enhancing drug efficacy.World journal of hepatology · 2025Review
- Retinol binding protein 4 enhances cellular cholesterol uptake to facilitate influenza A virus infection.PLoS pathogens · 2025Article
- A randomized controlled trial on the efficacy and safety of vitamin A supplementation in children with sepsis.Frontiers in pediatrics · 2025Article
- Strategic Optimization of the Middle Domain IIIA in RBP-Albumin IIIA-IB Fusion Protein to Enhance Productivity and Thermostability.International journal of molecular sciences · 2024Article
- Optimizing the Amino Acid Sequence Enhances the Productivity and Bioefficacy of the RBP-Albumin Fusion Protein.Bioengineering (Basel, Switzerland) · 2024Article
- Fusion Protein of RBP and Albumin Domain III Reduces Lung Fibrosis by Inactivating Lung Stellate Cells.Biomedicines · 2023Article
- Insights on drug and gene delivery systems in liver fibrosis.Asian journal of pharmaceutical sciences · 2023Review
- Fibrogenic Pathways in Metabolic Dysfunction Associated Fatty Liver Disease (MAFLD).International journal of molecular sciences · 2022Review
- Inhibition of Hepatic Stellate Cell Activation Suppresses Tumorigenicity of Hepatocellular Carcinoma in Mice.The American journal of pathology · 2021Article
- Albumin inhibits the nuclear translocation of Smad3 via interleukin-1beta signaling in hepatic stellate cells.Scientific reports · 2021Article
- Inhibition of Renal Stellate Cell Activation Reduces Renal Fibrosis.Biomedicines · 2020Article
- A pocket-escaping design to prevent the common interference with near-infrared fluorescent probes in vivo.Nature communications · 2020Article
- Targeted Drug Delivery to Hepatic Stellate Cells for the Treatment of Liver Fibrosis.The Journal of pharmacology and experimental therapeutics · 2019Review
- Targeted Delivery of an siRNA/PNA Hybrid Nanocomplex Reverses Carbon Tetrachloride-Induced Liver Fibrosis.Advanced therapeutics · 2019Article
- Galectin-1 gene silencing inhibits the activation and proliferation but induces the apoptosis of hepatic stellate cells from mice with liver fibrosis.International journal of molecular medicine · 2019Article
- Mining TCGA Database for Tumor Microenvironment-Related Genes of Prognostic Value in Hepatocellular Carcinoma.BioMed research international · 2019Article
- From targeted drug delivery to tissue regeneration: the evolving role of nanoparticle therapies in liver disease.Regenerative medicineArticle
Corrections and comments
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Authors and funding
14 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Activated hepatic stellate cells (HSCs) play a key role in liver fibrosis, and inactivating HSCs has been considered a promising therapeutic approach. We previously showed that albumin and its derivative designed for stellate cell-targeting, retinol-binding protein-albumin domain III fusion protein (referred to as R-III), inactivate cultured HSCs. Here, we investigated the mechanism of action of albumin/R-III in HSCs and examined the anti-fibrotic potential of R-III in vivo. R-III treatment and albumin expression downregulated retinoic acid (RA) signaling which was involved in HSC activation. RA receptor agonist and retinaldehyde dehydrogenase overexpression abolished the anti-fibrotic effect of R-III and albumin, respectively. R-III uptake into cultured HSCs was significantly decreased by siRNA-STRA6, and injected R-III was localized predominantly in HSCs in liver. Importantly, R-III administration reduced CCl4- and bile duct ligation-induced liver fibrosis. R-III also exhibited a preventive effect against CCl4-inducd liver fibrosis. These findings suggest that the anti-fibrotic effect of albumin/R-III is, at least in part, mediated by downregulation of RA signaling and that R-III is a good candidate as a novel anti-fibrotic drug.
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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.