2. Vascular Repair

  1. Gary S. Hoffman MD, MS7,
  2. Cornelia M. Weyand MD, PhD8,
  3. Carol A. Langford MD, MHS7 and
  4. Jörg J. Goronzy MD, PhD8
  1. Christian Troidl PhD1,
  2. Kerstin Troidl PhD2,3,
  3. Georg Jung2,3,
  4. Thomas Schmitz-Rixen MD, PhD4,5 and
  5. Wolfgang Schaper MD, PhD6

Published Online: 3 MAY 2012

DOI: 10.1002/9781118355244.ch2

Inflammatory Diseases of Blood Vessels, Second Edition

Inflammatory Diseases of Blood Vessels, Second Edition

How to Cite

Troidl, C., Troidl, K., Jung, G., Schmitz-Rixen, T. and Schaper, W. (2012) Vascular Repair, 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.ch2

Editor Information

  1. 7

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

  2. 8

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

Author Information

  1. 1

    Franz-Groedel-Institute, Kerckhoff Heart and Thorax Center, Bad Nauheim, Germany

  2. 2

    Department of Pharmacology, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany

  3. 3

    Department of Vascular and Endovascular Surgery, Goethe-University, Frankfurt am Main, Germany

  4. 4

    Department of Vascular and Endovascular Surgery, Goethe-University, Germany

  5. 5

    Department of Wound Care, Goethe University Hospital, Frankfurt am Main, Germany

  6. 6

    Department of Arteriogenesis Research, Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany

Publication History

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

ISBN Information

Print ISBN: 9781444338225

Online ISBN: 9781118355244



  • Arteriogenesis;
  • collateral arteries;
  • monocytes/macrophages;
  • MCP1;
  • ABRA;
  • TRPV4;
  • NOS;
  • fluid shear stress


Blood flow in obstructed arteries can be rerouted into developing vessels bypassing the occlusion. These vessels are small arterioles, part of a pre-existent arteriolar network, that expand by growth. Under the influence of increased fluid shear stress the endothelium is activated and bone marrow derived cells (monocytes) are attracted and invade the intima, digest the internal elastic lamina and activate smooth muscle cells (SMCs) of the media that proliferate and migrate and lead to the enlargement of the arteriole up to 10-fold of its initial diameter depending on the size of the animal or organ. Resting blood flow is restored within 1 week after arterial occlusion, but maximal conductance (blood flow reserve) reaches only 40% of normal. With artificially increased flow, as in shunts where collateral flow is rerouted into the venous system, complete normalization of maximal conductance is reached. In contrast to the coronary artery system where endothelial activation attracts monocytes, in peripheral collaterals, monocytes assemble mainly in the adventitia through the action of SMC generated MCP-1 and VCAM. In addition to this innate immune system activation, the molecular mechanisms guiding the transformation of functional resistance vessels into bulk flow carrying arteries include chronic shear stress involving the NO system. While other signaling pathways, like the Ras, -Raf, -Erk- and the Rho-pathway converge to aid in proliferation, the NOS system exerts the strongest influence: combined knockout/inhibition of eNOS+iNOS completely abolishes arteriogenesis. Exogenous application of NO donors facilitates collateral vessel formation. So far, selective delivery of substances or gene products to support local arteriogenesis remains a problem and the best therapeutic option are means to achieve high levels of blood flow.