ArticleMolecular biology reports2022
G-CSF promotes the viability and angiogenesis of injured liver via direct effects on the liver cells.
Article in Molecular biology reports, 2022. 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.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- A cigarette compound-induced tumor microenvironment promotes sorafenib resistance in hepatocellular carcinoma via the 14-3-3η-modified tumor-associated proteome.Chinese medical journal · 2026Article
- Functional Analysis of IL-6 Genetic Variants and Their Potential Role in Lipid Homeostasis and Inflammatory Regulation in Colombian Athletes.Current issues in molecular biology · 2026Article
- Effect and prognostic factors of the double plasma molecular adsorption system combined with partial plasma exchange (DPMAS-PPE) in patients with liver failure.Clinical and experimental hepatology · 2025Article
- Mimicking chronic alcohol effects through a controlled and sustained ethanol release device.Journal of biological engineering · 2024Article
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Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundPresently, liver transplantation is the only treatment strategy for liver failure (LF). Although granulocyte-colony stimulating factor (G-CSF) exhibits protective functions in LF, it is not clear whether it directly affects the liver cells. METHODS AND
resultsWe established an injured liver cell model and observed that G-CSF treatment promoted cell viability and enhanced Ki67 and VEGF-A expression. Thereafter, human umbilical vein endothelial cells (HUVECs) were cultured in a conditioned medium collected from the G-CSF-treated injured liver cells. HUVECs' proliferation and tubule formation were promoted. Furthermore, in an injured liver mouse model, confirmed via haematoxylin-eosin staining, we evaluated serum alanine aminotransferase activity, Ki67 expression, and microvessel density (MVD). G-CSF treatment significantly relieved liver injury, upregulated Ki67 expression, and enhanced MVD in the injured mouse liver tissue. Additionally, AKT and ERK signal targets were explored, and it was demonstrated that the effects of G-CSF on injured liver cells were mediated through the AKT and ERK signalling pathways.
conclusionsG-CSF promotes injured liver viability and angiogenesis by directly affecting injured liver cells via the AKT and ERK signalling pathways. These findings improve our understanding of the role of G-CSF in recovery from LF.
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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 Socratic graph.