ArticleBiological research2019
Notum attenuates HBV-related liver fibrosis through inhibiting Wnt 5a mediated non-canonical pathways.
Article in Biological research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The trial behind it
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Who cites it
9 citing papers in PubMed, 24 citations in OpenAlex.
- Review
- Molecular Network Analysis of HBV Persistent Infection from the Perspective of Whole Transcriptome.Biomolecules · 2025Article
- Wnt5a and Notum influence the temporal dynamics of cartilaginous mesenchymal condensations in developing trachea.Frontiers in cell and developmental biology · 2025Article
- Wnt5a/β-catenin-mediated epithelial-mesenchymal transition: a key driver of subretinal fibrosis in neovascular age-related macular degeneration.Journal of neuroinflammation · 2024Article
- Signaling pathways that activate hepatic stellate cells during liver fibrosis.Frontiers in medicine · 2024Review
- Associations of Wnt5a expression with liver injury in chronic hepatitis B virus infection.BMC infectious diseases · 2023Article
- Insights into the impact of hepatitis B virus on hepatic stellate cell activation.Cell communication and signaling : CCS · 2023Review
- NOTUM promotes thermogenic capacity and protects against diet-induced obesity in male mice.Scientific reports · 2021Article
- HBV induces liver fibrosis via the TGF-β1/miR-21-5p pathway.Experimental and therapeutic medicine · 2021Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 1 country.
Funding
Abstract
backgroundNon-canonical Wnt pathways play important roles in liver fibrosis. Notum is a newly discovered inhibitor to Wnt proteins. This study was to investigate anti-fibrotic effects of Notum.
methods53 patients with hepatitis B virus (HBV) infection as well as a cell co-culture system of LX-2 and Hep AD38 cells were engaged in this study. Clinical, biological and virological data of each patient were analyzed. Cell viability was detected at different time points. mRNA and protein levels of NFATc1 (Nuclear factor of activated T-cells), Jnk, α-SMA, Col1A1 and TIMP-1 were detected both in LX-2 and liver tissue. Protein levels of NFATc1 and Jnk in liver tissue and their correlations with fibrosis score were analyzed.
resultsHepatitis B virus replication up-regulated Wnt5a induced NFATc1 and Jnk activity in Hep AD38. Notum suppressed NFATc1, Jnk and fibrosis genes expression, reduced cell viability in co-cultured LX-2 cells induced by HBV. Interestingly, Patients with HBV DNA > 5log copies/ml had higher mRNA levels of NFATc1 and fibrosis genes than patients with HBV DNA < 5log copies/ml. Most importantly, protein expressions of NFATc1 and pJnk have positive correlations with liver fibrosis scores in HBV-infected patients.
conclusionsOur data showed that Notum inhibited HBV-induced liver fibrosis through down-regulating Wnt 5a mediated non-canonical pathways. This study shed light on anti-fibrotic treatment.
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