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- aggregation classification "A1".
- aggregation creator B866635.
- aggregation creator B866636.
- aggregation creator B866637.
- aggregation creator B866638.
- aggregation creator B866639.
- aggregation creator B866640.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
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- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation creator person.
- aggregation date "2013".
- aggregation format "application/pdf".
- aggregation hasFormat 3821138.bibtex.
- aggregation hasFormat 3821138.csv.
- aggregation hasFormat 3821138.dc.
- aggregation hasFormat 3821138.didl.
- aggregation hasFormat 3821138.doc.
- aggregation hasFormat 3821138.json.
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- aggregation hasFormat 3821138.mods.
- aggregation hasFormat 3821138.rdf.
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- aggregation hasFormat 3821138.txt.
- aggregation hasFormat 3821138.xls.
- aggregation hasFormat 3821138.yaml.
- aggregation isPartOf urn:issn:0270-9139.
- aggregation language "eng".
- aggregation rights "I have transferred the copyright for this publication to the publisher".
- aggregation subject "Biology and Life Sciences".
- aggregation title "Role of vascular endothelial growth factor in the pathophysiology of nonalcoholic steatohepatitis in two rodent models".
- aggregation abstract "The pathophysiology of nonalcoholic steatohepatitis (NASH) should be approached as a multifactorial process. In several stages of NASH, a link between disease progression and hepatic microvasculature changes can be made. In this study we investigated the role of angiogenesis in two mouse models for NASH, and the effect of a preventive and therapeutic antiangiogenic treatment in a diet-induced mouse model for NASH. Protein and RNA levels of angiogenic and inflammatory factors were significantly up-regulated in the liver of C56BL/6 and db/db mice with NASH at different timepoints. To examine the effect of angiogenic factors on the disease progression of NASH, a prevention and treatment study was set up, blocking the placental growth factor (PlGF) or vascular endothelial growth factor receptor 2 (VEGFR2). Our study showed that treatment prevents the progression of NASH by attenuating steatosis and inflammation, both in a preventive and therapeutic setting, thereby confirming the hypothesis that angiogenic factors play an early role in the disease progression from steatosis to NASH. Anti-PlGF (alpha PlGF) did not significantly improve liver histology. Vascular corrosion casting showed a more disrupted liver vasculature in mice with NASH compared to controls. Treatment with alpha VEGFR2 showed an improvement of the liver vasculature. Moreover, fat-laden primary hepatocytes treated with aVEGFR2 stored significantly less lipids. Conclusion: Our results demonstrate that there is an increased expression of angiogenic factors in the liver in different mouse models for NASH. We found that VEGFR2 blockage attenuates steatosis and inflammation in a diet-induced mouse model for NASH in a preventive and therapeutic setting. Our findings warrant further investigation of the role of angiogenesis in the pathophysiology in NASH.".
- aggregation authorList BK1244145.
- aggregation endPage "1805".
- aggregation issue "5".
- aggregation startPage "1793".
- aggregation volume "57".
- aggregation aggregates 3821154.
- aggregation isDescribedBy 3821138.
- aggregation similarTo hep.26219.
- aggregation similarTo LU-3821138.