ArticleOncotarget2017
Thymosin-β4 inhibits proliferation and induces apoptosis of hepatic stellate cells through PI3K/AKT pathway.
Article in Oncotarget, 2017. 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
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
5 citing papers in PubMed, 9 citations in OpenAlex.
- Thymosin Beta-4 Modulates Cardiac Remodeling by Regulating ROCK1 Expression in Adult Mammals.International journal of molecular sciences · 2025Article
- Thymosin Beta 4 Inhibits LPS and ATP-Induced Hepatic Stellate Cells via the Regulation of Multiple Signaling Pathways.International journal of molecular sciences · 2023Article
- Proteomic characterisation of prostate cancer intercellular communication reveals cell type-selective signalling and TMSB4X-dependent fibroblast reprogramming.Cellular oncology (Dordrecht, Netherlands) · 2022Article
- Role of phosphatidylinositol 3-kinase signaling pathway in radiation-induced liver injury.The Kaohsiung journal of medical sciences · 2020Article
- Semen Brassicae ameliorates hepatic fibrosis by regulating transforming growth factor-β1/Smad, nuclear factor-κB, and AKT signaling pathways in rats.Drug design, development and therapy · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver fibrosis is a necessary stage for chronic liver diseases, and serious threat to human health. Hepatic fibrosis is a necessary stage for chronic liver diseases. Hepatic stellate cells (HSCs) are the primary cell type responsible for fibrosis. Thymosin beta 4 (Tβ4) has a potential role in the pathogenesis of liver fibrosis and that it is especially associated with the activation of HSCs, however, the underlying mechanisms are not fully elucidated. Herein, we investigated the potential role of Tβ4 in liver fibrosis by describing the effects of Tβ4, and we discuss the possible signaling pathway regulated by Tβ4. The expression of Tβ4 was significantly decreased in human HSC cell line LX-2 and CCl4-treated mouse liver. The depletion of Tβ4 significantly associated with the activation of HSCs via the enhanced expression of α-SMA and vimentin. Tβ4 significantly suppressed the viability and migration of HSCs. Understanding the potential effects and regulatory mechanism of Tβ4 in liver fibrosis might help to provide a novel treatment for patients with 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.