ArticlePediatric cardiology2013
Endostatin, an inhibitor of angiogenesis, decreases after bidirectional superior cavopulmonary anastamosis.
Article in Pediatric cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 21 citations in OpenAlex.
- Recombinant human endostatin plus paclitaxel/nedaplatin for recurrent or metastatic advanced esophageal squamous cell carcinoma: a prospective, single-arm, open-label, phase II study.Investigational new drugs · 2021Trial
- Clinical practice variability among paediatric interventional cardiologists assessing pulmonary arteriovenous malformations.Cardiology in the young · 2025Article
- Pathophysiology of endothelial dysfunction in Fontan circulation: from bench to bedside and back again.Angiogenesis · 2025Review
- Quantitative plasma proteomic analysis in children after superior cavopulmonary anastomosis with pulmonary arteriovenous malformations.Pediatric research · 2025Article
- Pulmonary Vascular Sequelae of Palliated Single Ventricle Circulation: Arteriovenous Malformations and Aortopulmonary Collaterals.Journal of cardiovascular development and disease · 2022Review
- Hepatic factor may not originate from hepatocytes.Frontiers in cardiovascular medicine · 2022Article
- A Comparative Study of Invasive Modalities for Evaluation of Pulmonary Arteriovenous Fistula after Bidirectional Glenn Shunt.Pediatric cardiology · 2021Article
- Pulmonary vascular disease in Fontan circulation-is there a rationale for pulmonary vasodilator therapies?Cardiovascular diagnosis and therapy · 2021Review
- Angiopoietin-2 predicts morbidity in adults with Fontan physiology.Scientific reports · 2019Article
- Fontan Revision with Y-Graft in a Patient with Unilateral Pulmonary Arteriovenous Malformation.The Korean journal of thoracic and cardiovascular surgery · 2017Article
- Pulmonary arteriovenous malformations.American journal of respiratory and critical care medicine · 2014Review
- Pulmonary arteriovenous malformations after the superior cavopulmonary shunt: mechanisms and clinical implications.Expert review of cardiovascular therapy · 2014Review
- Pulmonary artery endothelial cell phenotypic alterations in a large animal model of pulmonary arteriovenous malformations after the Glenn shunt.The Annals of thoracic surgery · 2013Article
- Progressive cyanosis following Kawashima operation: slow resolution after redirection of hepatic veins.Journal of cardiothoracic surgery · 2013Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Pulmonary arteriovenous malformations (PAVMs) are a common source of morbidity after bidirectional superior cavopulmonary anastomosis (Glenn). The diversion of hepatic venous effluent away from the pulmonary circulation after Glenn appears to play a significant role in the pathogenesis of PAVMs. Although the liver is known to produce factors that regulate vascular development, specific hepatic inhibitors of angiogenesis have not been described in the post-Glenn population. Endostatin, produced from its precursor collagen XVIII, is a potent inhibitor of angiogenesis produced by the liver. This study aimed to investigate the hypothesis that endostatin levels decrease in patients after Glenn. Levels of endostatin and its precursor, long-type collagen XVIII, were determined by enzyme-linked immunoassay and immunoprecipitation, respectively, for serum samples from 38 patients undergoing Glenn, total cavopulmonary anastomosis (Fontan), or biventricular repair of cardiac defects. Samples were obtained before surgery and 24 h afterward. In patients undergoing a bidirectional Glenn procedure, endostatin levels decreased after surgery (n = 17; 4.42 vs 3.34 ng/ml; p < 0.001), and long type-collagen XVIII levels increased by 200 % (n = 10; p = 0.0001). However, endostatin levels did not change after surgery in patients undergoing Fontan (n = 13) or biventricular repair (n = 8). In patients undergoing Fontan, long-type collagen XVIII increased by 18 % (p < 0.01), whereas in control subjects, the levels were unchanged. These data suggest that the diversion of hepatic blood flow away from the pulmonary circulation in patients after the Glenn procedure inhibits endostatin production from collagen XVIII, resulting in decreased circulating serum endostatin levels. A decrease in endostatin may promote angiogenesis. The mechanism whereby the pulmonary circulation processes endostatin and its potential role in the pathogenesis of PAVMs warrant further study.
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