1. Vascular Development

  1. Gary S. Hoffman MD, MS3,
  2. Cornelia M. Weyand MD, PhD4,
  3. Carol A. Langford MD, MHS3 and
  4. Jörg J. Goronzy MD, PhD4
  1. Domenico Ribatti MD1 and
  2. Enrico Crivellato MD2

Published Online: 3 MAY 2012

DOI: 10.1002/9781118355244.ch1

Inflammatory Diseases of Blood Vessels, Second Edition

Inflammatory Diseases of Blood Vessels, Second Edition

How to Cite

Ribatti, D. and Crivellato, E. (2012) Vascular Development, in Inflammatory Diseases of Blood Vessels, Second Edition (eds G. S. Hoffman, C. M. Weyand, C. A. Langford and J. J. Goronzy), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781118355244.ch1

Editor Information

  1. 3

    Department of Rheumatic and Immunologic Diseases, Center for Vasculitis Care and Research, Cleveland Clinic, Lerner College of Medicine, Cleveland, OH, USA

  2. 4

    Department of Medicine, Stanford University School of Medicine, Stanford, CA, USA

Author Information

  1. 1

    Department of Basic Medical Sciences, Anatomy and Histology Section, University of Bari Medical School, Bari, Italy

  2. 2

    Department of Medical and Morphological Research, Anatomy Section, University of Udine Medical School, Udine, Italy

Publication History

  1. Published Online: 3 MAY 2012
  2. Published Print: 8 JUN 2012

ISBN Information

Print ISBN: 9781444338225

Online ISBN: 9781118355244



  • Endothelial cells;
  • vascular heterogeneity;
  • vascular diseases


Blood vessels represent an essential component of all organs. The vascular tree develops early during embryogenesis and progresses into a highly branched system of vascular channels lined by endothelial cells (ECs) and surrounded by mural cells. A highly hierarchical vascular architecture is established which comprises distinct arterial, capillary and venous segments as well as organ- and tissue-specific vascular beds. Several factors are involved in these processes, such as vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF), transforming growth factor beta (TGF-β), angiopoietins, (Ang) and ephrins (Efn). EC structural and molecular heterogeneity plays a crucial role in patterning the distinct segments of the blood vessel architecture. It is possible that EC heterogeneity has a role in directing disease processes to distinct vascular territories. Vice versa, vascular inflammatory disease may have different downstream consequences for EC function in different territories. Defining the molecular basis for the targeting of systemic vasculitides, thrombotic or haemorrhagic conditions, sepsis reactions, and metabolic vascular diseases is subject to ongoing research. Much progress has been made in understanding the molecular pathways that regulate fate decisions of precursor cells to develop into arterial or venous EC. Identification of vascular-bed specific structural and molecular profiles will contribute to a better definition of the complexity of the angioarchitecture. Characterization of the molecules involved in creating vascular heterogeneity might eventually allow refinement of diagnostic and therapeutic strategies aimed at targeting distinct segments of the vascular tree.