ArticleNature communications2016
CUG-binding protein 1 regulates HSC activation and liver fibrogenesis.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Curriculum vitae of CUG binding protein 1 (CELF1) in homeostasis and diseases: a systematic review.Cellular & molecular biology letters · 2024Pooled it
- Contribution of p38 MAPK in liver fibrosis: An overview of mechanisms, signaling pathways, and therapeutic targets (Review).International journal of molecular medicine · 2026Review
- Macrophage FOLR2 drives liver fibrosis via intercellular engagement of TGFβRII.Acta pharmacologica Sinica · 2026Article
- ZFP36 Alleviates MASLD Through Facilitating TEAD4 mRNA Degradation After Sleeve Gastrectomy.International journal of molecular sciences · 2026Article
- Glycyrrhizin preparations in liver diseases: a narrative review of mechanisms and therapeutic potential.Frontiers in pharmacology · 2026Review
- A novel feedback loop: CELF1/circ-CELF1/BRPF3/KAT7 in cardiac fibrosis.Acta pharmaceutica Sinica. B · 2025Article
- Adipocyte RNA-binding protein CELF1 promotes beiging of white fat through stabilizing Dio2 mRNA.Nature communications · 2025Article
- Fraxinellone-mediated targeting of cathepsin B leakage from lysosomes induces ferroptosis in fibroblasts to inhibit hypertrophic scar formation.Biology direct · 2025Article
- An Autologous Macrophage-Based Phenotypic Transformation-Collagen Degradation System Treating Advanced Liver Fibrosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Dysregulation of RNA splicing in early non-alcoholic fatty liver disease through hepatocellular carcinoma.Scientific reports · 2024Article
- Natural compound fraxinellone ameliorates intestinal fibrosis in mice via direct intervention of HSP47-collagen interaction in the epithelium.Acta pharmacologica Sinica · 2023Article
- Remodeling of the liver fibrosis microenvironment based on nilotinib-loaded multicatalytic nanozymes with boosted antifibrogenic activity.Acta pharmaceutica Sinica. B · 2023Article
- Tissue fibrosis induced by radiotherapy: current understanding of the molecular mechanisms, diagnosis and therapeutic advances.Journal of translational medicine · 2023Review
- Heterotypic signaling of cancer-associated fibroblasts in shaping the cancer cell drug resistance.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- Antihepatofibrotic effect of Guizhifuling pill on carbon tetrachloride-induced liver fibrosis in mice.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2022Article
- Inhibition of ASCT2 induces hepatic stellate cell senescence with modified proinflammatory secretome through an IL-1Acta pharmaceutica Sinica. B · 2022Article
- The m6A reader YTHDF3-mediated PRDX3 translation alleviates liver fibrosis.Redox biology · 2022Article
- Guizhi Fuling pill attenuates liver fibrosisBioengineered · 2022Article
- Small molecule targeting CELF1 RNA-binding activity to control HSC activation and liver fibrosis.Nucleic acids research · 2022Article
- Natural Compounds Targeting Cancer-Associated Fibroblasts against Digestive System Tumor Progression: Therapeutic Insights.Biomedicines · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive activation of hepatic stellate cells (HSCs) is a key step in liver fibrogenesis. Here we report that CUG-binding protein 1 (CUGBP1) expression is elevated in HSCs and positively correlates with liver fibrosis severity in human liver biopsies. Transforming growth factor-beta (TGF-β) selectively increases CUGBP1 expression in cultured HSCs in a p38 mitogen-activated protein kinase (MAPK)-dependent manner. Knockdown of CUGBP1 inhibits alpha smooth muscle actin (α-SMA) expression and promotes interferon gamma (IFN-γ) production in HSCs in vitro. We further show that CUGBP1 specifically binds to the 3' untranslated region (UTR) of human IFN-γ mRNA and promotes its decay. In mice, knockdown of CUGBP1 alleviates, whereas its overexpression exacerbates, bile duct ligation (BDL)-induced hepatic fibrosis. Therefore, CUGBP1-mediated IFN-γ mRNA decay is a key event for profibrotic TGF-β-dependent activation of HSCs, and inhibiting CUGBP1 to promote IFN-γ signalling in activated HSCs could be a novel strategy to treat liver fibrosis.
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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.