| Article ID | Journal | Published Year | Pages | File Type | 
|---|---|---|---|---|
| 2873142 | The Annals of Thoracic Surgery | 2013 | 8 Pages | 
Abstract
												These findings demonstrate that PAVMs developed in a clinically relevant animal model of SCPC concomitantly with differential changes in PAEC proliferative ability and phenotype. Moreover, there was a significant increase in the angiopoietin/Tie-2 complex in the right lung, which may provide novel therapeutic targets to attenuate PAVM formation after a SCPC.
											Keywords
												ECMPAECPAVMRPASMCSuperior cavopulmonary connectionSCPCLPAHIFcycle thresholdpulmonary artery endothelial cellSmooth muscle cellEndothelial cellPulmonary arteryright pulmonary arteryLeft pulmonary arteryVascular endothelial growth factorVascular Endothelial Growth Factor (VEGF)Hypoxia Inducible FactorExtracellular matrixAVMPulmonary arteriovenous malformationArteriovenous malformations
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											Authors
												Minoo N. MD, Rupak PhD, Shaina R. MD, William F. BS, Christina BS, Robert E. MS, Risha K. BS, Elizabeth K. BS, Francis G. MD, PhD, Eric M. MD, Geoffrey A. MD, Scott M. MD, John S. MD, PhD, Jeffrey A. PhD, 
											