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(Circulation Research. 2009;104:576.)
© 2009 American Heart Association, Inc.

Review

Arterial–Venous Specification During Development

Matthew R. Swift, Brant M. Weinstein

From the Laboratory of Molecular Genetics, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Md.

Correspondence to Brant M. Weinstein, Laboratory of Molecular Genetics, NICHD, NIH, Building 6B, Room 309, 6 Center Dr, Bethesda, MD 20892. E-mail flyingfish{at}nih.gov

This Review is part of a thematic series on Arterial Specification: A Finishing School for the Endothelium, which includes the following articles:

Role of Crosstalk Between Phosphatidylinositol 3-Kinase and Extracellular Signal-Regulated Kinase/Mitogen-Activated Protein Kinase Pathways in Artery–Vein Specification [2008;103:573–579]

Branching Morphogenesis [2008;103:784–795]

Brothers and Sisters: Molecular Insights Into Arterial–Venous Heterogeneity [2008;103:929–939]

Shared Circuitry: Developmental Signaling Cascades Regulate Both Embryonic and Adult Coronary Vasculature [2009;104:159–169]

Guidance of Vascular Development: Lessons From the Nervous System [2009;104:428–441]

Arterial–Venous Specification During Development
Michael Simons Guest Editor

The major arteries and veins of the vertebrate circulatory system are formed early in embryonic development, before the onset of circulation, following de novo aggregation of "angioblast" progenitors in a process called vasculogenesis. Initial embryonic determination of artery or vein identity is regulated by variety of genetic factors that work in concert to specify endothelial cell fate, giving rise to 2 distinct components of the circulatory loop possessing unique structural characteristics. Work in multiple in vivo animal model systems has led to a detailed examination of the interacting partners that determine arterial and venous specification. We discuss the hierarchical arrangement of many signaling molecules, including Hedgehog (Hh), vascular endothelial growth factor (VEGF), Notch, and chicken ovalbumin upstream-transcription factor II (COUP-TFII) that promote or inhibit divergent pathways of endothelial cell fate. Elucidation of the functional role of these genetic determinants of blood vessel specification together with the epigenetic factors involved in subsequent modification of arterial–venous identity will allow for potential new therapeutic targets for vascular disorders.

Key Words: arterial–venous specification • Hh • VEGF • Notch • COUP-TFII

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