ArticleCells2019
Characterization of the Roles of Vimentin in Regulating the Proliferation and Migration of HSCs during Hepatic Fibrogenesis.
Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- HIF-2α induction in de novo lipogenesis in metabolic dysfunction-associated steatohepatitis is dependent on IL-21 signaling.The Journal of biological chemistry · 2026Article
- Spatial phosphoproteomics reveals regional phosphorylation features in liver cirrhosis progression.Journal of translational medicine · 2026Article
- Progressive fibrosis in human MASLD is associated with spatially linked transcriptomic signatures of metabolic reprogramming and senescence.JHEP reports : innovation in hepatology · 2026Article
- Dynamic cholangiocyte responses in a murine model of reversible cholestasis: macrophage remodeling and NF-Y-mediated TGFβ1 expression.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Comprehensive Genetic and Molecular Characterization Confirms Hepatic Stellate Cell Origin of the Immortal Col-GFP HSC Line.International journal of molecular sciences · 2025Article
- Article
- TRIM47 promotes hypopharyngeal and laryngeal cancers progression through promoting K63-linked ubiquitination of vimentin.Cancer science · 2025Article
- miR-106b-5p protects against drug-induced liver injury by targeting vimentin to stimulate liver regeneration.MedComm · 2024Article
- Distinctive protein expression in elderly livers in a Sprague-Dawley rat model of normothermic ex vivo liver machine perfusion.European journal of medical research · 2024Article
- Mechanobiology in Metabolic Dysfunction-Associated Steatotic Liver Disease and Obesity.Current issues in molecular biology · 2024Review
- FRMD3 inhibits the growth and metastasis of breast cancer through the ubiquitination-mediated degradation of vimentin and subsequent impairment of focal adhesion.Cell death & disease · 2023Article
- Article
- Liver pathology and biochemistry in patients with mutations in TRIM37 gene (Mulibrey nanism).Liver international : official journal of the International Association for the Study of the Liver · 2022Article
- Article
- Impact of Vimentin on Regulation of Cell Signaling and Matrix Remodeling.Frontiers in cell and developmental biology · 2022Review
- Comparative Analysis of Dental Pulp and Periodontal Stem Cells: Differences in Morphology, Functionality, Osteogenic Differentiation and Proteome.Biomedicines · 2021Article
- Molecular characterization and cell type composition deconvolution of fibrosis in NAFLD.Scientific reports · 2021Article
- Resolvin D1 attenuates CCl4 Induced Liver Fibrosis by Inhibiting Autophagy-Mediated HSC activationFrontiers in pharmacology · 2021Article
- Characterizing the Relapse Potential in Different Luminal Subtypes of Breast Cancers with Functional Proteomics.International journal of molecular sciences · 2020Article
- Water-Soluble Pristine CPharmaceutics · 2020Article
Corrections and comments
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Authors and funding
6 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The activation of hepatic stellate cells (HSCs) manifested as proliferation and migration is the pivotal event involved in liver fibrogenesis. The vimentin network, an intermediate filament (IF) system, is one of the critical cascades by which the cell morphology, growth, and motility are modulated. However, the vimentin-mediated cytoskeletal cross talk, as well as the signaling transduction, which further coordinates the cellular responses during hepatic fibrogenesis, is poorly understood. In the current study, both messenger RNA (mRNA) and the vimentin protein were significantly increased in a time-dependent manner in the dimethylnitrosamine (DMN)-exposed liver. In particular, vimentin was highly expressed in the activated HSCs. Again, the overexpressed vimentin was observed in the plasma samples derived from patients with hepatic fibrosis/cirrhosis, suggesting that vimentin may be a key factor in regulating the progression of liver fibrosis. Meanwhile, vimentin knockdown suppressed the migratory propensity, provoked morphological changes, and disturbed the focal adhesions in the HSCs due to the breakdown of associated cytoskeletal proteins. Western blotting showed that vimentin deletion inhibited proliferating cell nuclear antigen (PCNA) and arrested the Rho GTPase family, thereby impairing the HSCs' growth as well as motility. The phosphorylated extracellular-signal regulated kinase (ERK) and AKT signals were also notably reduced in response to the silence of vimentin. Inhibitors of selected signaling pathways suppressed the migration and differentiation of activated HSCs by regulating specific serine phosphorylated sites on vimentin. Taken together, these findings revealed a novel mechanism of vimentin through which various signaling pathways controlled the proliferation, differentiation, and movement of the HSCs via the ERK/AKT and Rho cascades.
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