ArticleJournal of cell communication and signaling2024
Survivin inhibition ameliorates liver fibrosis by inducing hepatic stellate cell senescence and depleting hepatic macrophage population.
Article in Journal of cell communication and signaling, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Polyploid Giant Cancer Cells as a Senescence-Linked State in the Tumor Microenvironment.Cancers · 2026Review
- Sexual Dimorphism in the Initial Apoptotic Switch During MASH Progression in Mice.International journal of molecular sciences · 2026Article
- Prognostic value of lymphatic vessel density in the capsule of early-stage hepatocellular carcinoma: implications for postoperative recurrence risk.Frontiers in immunology · 2026Article
- Evaluation of the effect of a single dose of morroniside on rat liver subjected to ischemia and reperfusion.Frontiers in molecular biosciences · 2026Article
- Survivin modulates stiffness-induced vascular smooth muscle cell motility.APL bioengineering · 2025Article
Corrections and comments
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Authors and funding
6 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Persistent activation of hepatic stellate cells (HSCs) in the injured liver leads to the progression of liver injury from fibrosis to detrimental cirrhosis. In a previous study, we have shown that survivin protein is upregulated during the early activation of HSCs, which triggers the onset of liver fibrosis. However, the therapeutic potential of targeting survivin in a fully established fibrotic liver needs to be investigated. In this study, we chemically induced hepatic fibrosis in mice using carbon tetrachloride (CCl4) for 6 weeks, which was followed by treatment with a survivin suppressant (YM155). We also evaluated survivin expression in fibrotic human liver tissues, primary HSCs, and HSC cell line by histological analysis. αSMA
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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.