ArticleBioMed research international2014
Toxic damage increases angiogenesis and metastasis in fibrotic livers via PECAM-1.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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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.
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Who cites it
15 citing papers in PubMed, 17 citations in OpenAlex.
- Integrated Network and Transcriptomic Analyses Identify a Candidate Ethanol-ADAM17 Molecular Axis Associated with Glioblastoma Progression.International journal of molecular sciences · 2026Article
- Discovery of novel biomarkers associated with myocardial fibrosis in chimpanzees (Frontiers in veterinary science · 2026Article
- Elucidating the role of IgA plasma cells and PECAM1-CD38 interaction in intestinal fibrosis: a single-cell RNA sequencing analysis in Crohn's disease.BMC gastroenterology · 2025Article
- Key Transcription Factors: Avenue for Treating Alcoholic Liver Disease.Current medical science · 2025Review
- TANGO6 regulates cell proliferation via COPI vesicle-mediated RPB2 nuclear entry.Nature communications · 2024Article
- Transcriptional regulation of alcohol induced liver fibrosis in a translational porcine hepatocellular carcinoma model.Biochimie · 2021Article
- Therapeutic and Protective Effects of Liposomal Encapsulation of Astaxanthin in Mice with Alcoholic Liver Fibrosis.International journal of molecular sciences · 2019Article
- Development of A New Mouse Model for Intrahepatic Cholangiocellular Carcinoma: Accelerating Functions of Pecam-1.Cancers · 2019Article
- Role of HIF-1α in Alcohol-Mediated Multiple Organ Dysfunction.Biomolecules · 2018Review
- Angiogenesis and Hepatic Fibrosis: Western and Chinese Medicine Therapies on the Road.Chinese journal of integrative medicine · 2018Review
- Circulating Endothelial Progenitor Cells Present an Inflammatory Phenotype and Function in Patients With Alcoholic Liver Cirrhosis.Frontiers in physiology · 2018Article
- Inhibition of vascular endothelial growth factor signaling facilitates liver repair from acute ethanol-induced injury in zebrafish.Disease models & mechanisms · 2016Article
- Oxidative stress in retinal pigment epithelium cells increases exosome secretion and promotes angiogenesis in endothelial cells.Journal of cellular and molecular medicine · 2016Article
- Statins activate the canonical hedgehog-signaling and aggravate non-cirrhotic portal hypertension, but inhibit the non-canonical hedgehog signaling and cirrhotic portal hypertension.Scientific reports · 2015Article
- Angiogenesis and liver fibrosis.World journal of hepatology · 2015Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive ethanol consumption is one of the main causes of liver fibrosis. However, direct effects of ethanol exposure on endothelial cells and their contribution to fibrogenesis and metastasis were not investigated. Therefore we analysed whether ethanol directly affects endothelial cells and if this plays a role during fibrogenesis and metastasis in the liver. Murine and human endothelial cells were exposed to ethanol for up to 72 hours. In vitro, effects on VEGF, HIF-1alpha, PECAM-1, and endothelial cell functions were analysed. In vivo, effects of continuous liver damage on blood vessel formation and metastasis were analysed by PECAM-1 immunohistochemistry. Ethanol increased HIF-1alpha and VEGF levels in murine and human endothelial cells. This resulted in enhanced intracellular signal transduction, and PECAM-1 expression as well as tube formation and wound healing. In vivo, toxic liver damage increased angiogenesis during fibrogenesis. Metastasis was also enhanced in fibrotic livers and located to PECAM-1 positive blood vessels compared to nonfibrotic mice. In conclusion, ethanol had strong effects on endothelial cells, which--at least in part--led to a profibrotic and prometastatic environment mediated by PECAM-1. Blockade of increased PECAM-1 expression could be a promising tool to inhibit fibrogenesis and metastasis in the liver.
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Registered trials
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