ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2014
The role of receptor tyrosine kinase activation in cholangiocytes and pulmonary vascular endothelium in experimental hepatopulmonary syndrome.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 43 citations in OpenAlex.
- Sorafenib in Hepatopulmonary Syndrome: A Randomized, Double-Blind, Placebo-Controlled Trial.Liver transplantation : official publication of the American Association for the Study of Liver Diseases and the International Liver Transplantation Society · 2019Trial
- Precision inflammation targeting via myeloperoxidase mediated antioxidant melanin nanomedicines for chronic inflammation therapy.Nature communications · 2026Article
- Agrimoniin ameliorates intrapulmonary angiogenesis and improves hypoxemia in hepatopulmonary syndrome via PGC-1α activation and glycolysis down-regulation.Genes & diseases · 2026Article
- Disruption of Hepatic Sinusoidal Homeostasis Leads to Hepatopulmonary Syndrome.Journal of cellular and molecular medicine · 2025Review
- Impact of hepatopulmonary syndrome in liver transplantation candidates and the role of angiogenesis.The European respiratory journal · 2022Article
- Endothelial glycocalyx in hepatopulmonary syndrome: An indispensable player mediating vascular changes.Frontiers in immunology · 2022Review
- [Diagnosis and therapeutic strategies for hepatopulmonary syndrome].Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of hepatology · 2020Article
- A high-dose rapamycin treatment alleviates hepatopulmonary syndrome in cirrhotic rats.Journal of the Chinese Medical Association : JCMA · 2020Article
- Krüppel-like factor 6 mediates pulmonary angiogenesis in rat experimental hepatopulmonary syndrome and is aggravated by bone morphogenetic protein 9.Biology open · 2019Article
- Melatonin effects on pulmonary tissue in the experimental model of Hepatopulmonary Syndrome.Jornal brasileiro de pneumologia : publicacao oficial da Sociedade Brasileira de Pneumologia e Tisilogia · 2019Article
- Chronic Hepatitis C with Cyanosis.Case reports in hepatology · 2019Article
- Potential Clinical Targets in Hepatopulmonary Syndrome: Lessons From Experimental Models.Hepatology (Baltimore, Md.) · 2018Review
- Review article: Update on current and emergent data on hepatopulmonary syndrome.World journal of gastroenterology · 2018Review
- Characterization of pressure-mediated vascular tone in resistance arteries from bile duct-ligated rats.Oncotarget · 2017Article
- Hepatopulmonary syndrome: What we know and what we would like to know.World journal of gastroenterology · 2016Review
- Quercetin alleviates pulmonary angiogenesis in a rat model of hepatopulmonary syndrome.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2016Article
- Hepatopulmonary Syndrome and Liver Transplantation: A Recent Review of the Literature.Journal of clinical and translational hepatology · 2016Review
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Authors and funding
7 authors at 3 institutions in 1 country.
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Abstract
Pulmonary vascular dilation and angiogenesis underlie experimental hepatopulmonary syndrome (HPS) induced by common bile duct ligation (CBDL) and may respond to receptor tyrosine kinase (RTK) inhibition. Vascular endothelial growth factor-A (VEGF-A) expression occurs in proliferating cholangiocytes and pulmonary intravascular monocytes after CBDL, the latter contributing to angiogenesis. CBDL cholangiocytes also produce endothelin-1 (ET-1), which triggers lung vascular endothelin B receptor-mediated endothelial nitric oxide synthase (eNOS) activation and pulmonary intravascular monocyte accumulation. However, whether RTK pathway activation directly regulates cholangiocyte and pulmonary microvascular alterations in experimental HPS is not defined. We assessed RTK pathway activation in cholangiocytes and lung after CBDL and the effects of the type II RTK inhibitor sorafenib in experimental HPS. Cholangiocyte VEGF-A expression and ERK activation accompanied proliferation and increased hepatic and circulating ET-1 levels after CBDL. Sorafenib decreased each of these events and led to a reduction in lung eNOS activation and intravascular monocyte accumulation. Lung monocyte VEGF-A expression and microvascular Akt and ERK activation were also found in vivo after CBDL, and VEGF-A activated Akt and ERK and angiogenesis in rat pulmonary microvascular endothelial cells in vitro. Sorafenib inhibited VEGF-A-mediated signaling and angiogenesis in vivo and in vitro and improved arterial gas exchange and intrapulmonary shunting. RTK activation in experimental HPS upregulates cholangiocyte proliferation and ET-1 production, leading to pulmonary microvascular eNOS activation, intravascular monocyte accumulation, and VEGF-A-mediated angiogenic signaling pathways. These findings identify a novel mechanism in cholangiocytes through which RTK inhibition ameliorates experimental HPS.
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