Alternatively spliced tissue factor promotes plaque angiogenesis through the activation of hypoxia-inducible factor-1α and vascular endothelial growth factor signaling.

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Published in Circulation on August 12, 2014

Authors

Chiara Giannarelli1, Matilde Alique2, David T Rodriguez2, Dong Kwon Yang2, Dongtak Jeong2, Claudia Calcagno2, Randolph Hutter2, Antoine Millon2, Jason C Kovacic2, Thomas Weber2, Peter L Faries2, Gerald A Soff2, Zahi A Fayad2, Roger J Hajjar2, Valentin Fuster2, Juan J Badimon2

Author Affiliations

1: From the AtheroThrombosis Research Unit (C.G., M.A., D.T.R., J.J.B.), Cardiovascular Research Institute (C.G., D.K.Y., D.J., J.C.K., T.W., R.J.H., V.F.), Translational and Molecular Imaging Institute (C.C., A.M., Z.A.F.), Department of Radiology (C.C., A.M., Z.A.F.), and Vascular Surgery (P.L.F.), Icahn School of Medicine at Mount Sinai, New York, NY; Memorial Sloan-Kettering, New York, NY (G.A.S.); and CNIC, Madrid, Spain (V.F.). chiara.giannarelli@mssm.edu.
2: From the AtheroThrombosis Research Unit (C.G., M.A., D.T.R., J.J.B.), Cardiovascular Research Institute (C.G., D.K.Y., D.J., J.C.K., T.W., R.J.H., V.F.), Translational and Molecular Imaging Institute (C.C., A.M., Z.A.F.), Department of Radiology (C.C., A.M., Z.A.F.), and Vascular Surgery (P.L.F.), Icahn School of Medicine at Mount Sinai, New York, NY; Memorial Sloan-Kettering, New York, NY (G.A.S.); and CNIC, Madrid, Spain (V.F.).

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