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Autor     Melany C. van Oostrom, Olivia van Oostrom, Paul H. A. Quax, Marianne C. Verhaar, Imo E. Hoefer
Titel    Insights into mechanisms behind arteriogenesis: what does the future hold?
Zeitschrift    Journal of Leukocyte Biology
Ausgabe    84
Datum    December 2008
Seiten    1379-1391
DOI    10.1189/jlb.0508281
URL    http://www.jleukbio.org/content/84/6/1379.full.pdf

Literaturverz.   

ja
Fußnoten    ja
Fragmente    8


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Cardiovascular disorders are currently the leading cause of death globally. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients who do not benefit from these treatment options. For a long time, it has been known that patients suffering from coronary heart disease can recruit collateral vessels and thereby improve symptoms of myocardial ischemia[1]. Also, it is well established that an increased demand for oxygen, as occurs during exercise and placental development, can induce formation of new capillaries[2]. Thus, it seems that the body already possesses an “in-house” rescue system to increase blood flow in ischemic circumstances. Stimulation of this system, termed neovascularization, could be a promising new direction in treating cardiovascular diseases[3]. Neovascularization in humans can be brought about by three distinct mechanisms: vasculogenesis, angiogenesis, or arteriogenesis (depicted in Fig. 1.1.)[3].

1. Helfant, R.H., P.S. Vokonas, and R. Gorlin, Functional importance of the human coronary collateral circulation. N Engl J Med, 1971. 284(23): p. 1277-81.

2. Prior, B.M., H.T. Yang, and R.L. Terjung, What makes vessels grow with exercise training? J Appl Physiol, 2004. 97(3): p. 1119-28.

3. Carmeliet, P., Mechanisms of angiogenesis and arteriogenesis. Nat Med, 2000. 6(4): p. 389-95.

In fact, cardiovascular disorders are currently the leading cause of death globally [1]. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients who do not benefit from these treatment options.

For a long time, it has been known that patients suffering from coronary heart disease can recruit collateral vessels and thereby improve symptoms of myocardial ischemia [2]. Also, it is well established that an increased demand in oxygen, as occurs during exercise and placental development, can induce formation of new capillaries [3]. Thus, it seems that the body already possesses an “in-house” rescue system to increase blood flow in ischemic circumstances. Stimulation of this system, termed neovascularization, could be a promising new direction in treating cardiovascular diseases. Neovascularization in humans can be fulfilled by three distinct mechanisms: vasculogenesis, angiogenesis, or arteriogenesis (depicted in Fig. 1) [4].


1. World Health Organization (February 2007) Factsheet 317.

2. Helfant, R. H., Vokonas, P. S., Gorlin, R. (1971) Functional importance of the human coronary collateral circulation. N. Engl. J. Med. 284, 1277–1281.

3. Prior, B. M., Yang, H. T., Terjung, R. L. (2004) What makes vessels grow with exercise training? J. Appl. Physiol. 97, 1119–1128.

4. Carmeliet, P. (2000) Mechanisms of angiogenesis and arteriogenesis. Nat. Med. 6, 389–395.

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The term “arteriogenesis”—the development of large collateral arteries from pre-existing arteriolar anastomoses—was proposed in 1997 by W. Schaper, R. Chapuli-Munoz, and W. Risau[7] to discriminate between arteriogenesis and true angiogenesis.

7. Ito, W.D., et al., Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am J Physiol, 1997. 273(3 Pt 2): p. H1255-65.

The term “arteriogenesis”—the development of large collateral arteries from pre-existing arteriolar anastomoses—was proposed in 1997 by W. Schaper, R. Chapuli-Munoz, and W. Risau [10] to discriminate between arteriogenesis and true angiogenesis.

10. Ito, W. D., Arras, M., Scholz, D., Winkler, B., Htun, P., Schaper, W. (1997) Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am. J. Physiol. 273, H1255–H1265.

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Fig. 1.1.

Haw 02a diss.png

[6] (Van Oostrom, M.C., et al., J Leukoc Biol, 2008;84(6): 1379-91)

Fig.1.1. Neovascularization can occur via vasculogenesis (A), angiogenesis (B), or arteriogenesis (C). (A) In vasculogenesis, circulating endothelial progenitor cells (EPC; purple) contribute to new blood vessel growth (capillaries). (B) During angiogenesis, endothelial cells are activated by ischemia and develop a lumen, thereby forming a new, small capillary vessel[3]. (C) In arteriogenesis, circulating leukocytes (green) are attracted to the activated endothelium. They assist in enlarging collateral anastomoses. Activated endothelial cells (blue), activated vascular smooth muscle cells (yellow)[3].

Normally, there is only a minimal net flow in these pre-existing connections. However, a sudden arterial occlusion or a slow progressing stenosis in the main artery can cause an increased pressure gradient in these small vessels to respond by actively proliferating and remodeling, which results in an increased lumen size and enhanced [perfusion to the ischemic tissue[20]. Hence, it seems that arteriogenesis is initiated differently and progresses differently from angiogenesis.]


3. Carmeliet, P., Mechanisms of angiogenesis and arteriogenesis. Nat Med, 2000. 6(4): p. 389-95.

6. van Oostrom, M.C., et al., Insights into mechanisms behind arteriogenesis: what does the future hold? J Leukoc Biol, 2008. 84(6): p. 1379-91.

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

Haw 02a source.png

Fig. 1. Neovascularization can occur via vasculogenesis (A), angiogenesis (B), or arteriogenesis (C). (A) In vasculogenesis, circulating endothelial progenitor cells (EPC; purple) contribute to new blood vessel growth (capillaries) by secreting the necessary growth factors and chemokines for endothelial cells to migrate (upper) or by incorporating into the newly formed vessels (lower). (B) During angiogenesis, endothelial cells are activated by ischemia and grow in the direction of angiogenic signals. The endothelial cells fuse and develop a lumen, thereby forming a new, small capillary vessel. (C) In arteriogenesis, circulating leukocytes (green) are attracted to the activated endothelium. They assist in enlarging collateral anastomoses. Activated endothelial cells (blue), activated vascular smooth muscle cells (yellow), quiescent endothelial cells (gray), quiescent smooth muscle cells (brown).

[...]

Normally, as a result of the high resistance of arteriolar anastomoses and the lack of a pressure gradient, there is only a minimal net flow in these pre-existing connections. However, a sudden arterial occlusion or a slow progressing stenosis in the main artery can cause an increased pressure gradient in the anastomoses, leading to increased blood flow inside. These small vessels respond by actively proliferating and remodeling, which results in an increased lumen size and enhanced perfusion to the ischemic tissue [11]. Hence, it seems that arteriogenesis is initiated differently and progresses differently to angiogenesis.


11. Schaper, W., Scholz, D. (2003) Factors regulating arteriogenesis. Arterioscler. Thromb. Vasc. Biol. 23, 1143–1151.

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Furthermore, FSS is almost impossible to measure in small collaterals. Pipp and colleagues[44] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic force in collateral growth.

Collaterals increase their diameter up to 20 times during arteriogenesis, which is possible through mitosis of vascular cells[45]. Given that the collateral vessels grow in length as well as in width, the expanding vessel arranges itself in loops and turns to accommodate the extra length. This gives the vessels a typical corkscrew pattern and causes energy loss[10].


10. Heil, M., et al., Arteriogenesis versus angiogenesis: similarities and differences. J Cell Mol Med, 2006. 10(1): p. 45-55.

44. Pipp, F., et al., Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hindlimb. Arterioscler Thromb Vasc Biol, 2004. 24(9): p. 1664-8.

45. Wolf, C., et al., Vascular remodeling and altered protein expression during growth of coronary collateral arteries. J Mol Cell Cardiol, 1998. 30(11): p. 2291-305.

Furthermore, FSS is almost impossible to measure in small collaterals.

[Seite 1381]

Pipp and colleagues [14] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further, significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic power in collateral growth.

Collaterals increase their diameter up to 20 times during arteriogenesis, which is possible through mitosis of vascular cells [15]. Given that the collateral vessels grow in length as well as in width, the expanding vessel arranges itself in loops and turns to accommodate the extra length. This gives the vessels a typical corkscrew pattern [16] and causes energy loss.


14. Pipp, F., Boehm, S., Cai, W. J., Adili, F., Ziegler, B., Karanovic, G., Ritter, R., Balzer, J., Scheler, C., Schaper, W., Schmitz-Rixen, T. (2004) Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. Arterioscler. Thromb. Vasc. Biol. 24, 1664–1668.

15. Wolf, C., Cai, W. J., Vosschulte, R., Koltai, S., Mousavipour, D., Scholz, D., Afsah-Hedjri, A., Schaper, W., Schaper, J. (1998) Vascular remodeling and altered protein expression during growth of coronary collateral arteries. J. Mol. Cell. Cardiol. 30, 2291–2305.

16. Heil, M., Eitenmuller, I., Schmitz-Rixen, T., Schaper, W. (2006) Arteriogenesis versus angiogenesis: similarities and differences. J. Cell. Mol. Med. 10, 45–55.

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[This, together with the premature arrest of arteriogenic growth,] as a result of the drop in FSS in the growing collateral, is a reason that collateral arteries cannot completely compensate the conductance of the artery they have replaced. Initially, during arteriogenesis, several collateral vessels are recruited and proliferate. However, as it is hemodynamically more efficient for fewer, larger arteries to conduct the blood than a greater number of smaller arteries, the smaller vessels regress later on, and those with the higher shear forces continue growing[46].

46. Hoefer, I.E., J.J. Piek, and G. Pasterkamp, Pharmaceutical interventions to influence arteriogenesis: new concepts to treat ischemic heart disease. Curr Med Chem, 2006. 13(9): p. 979-87.

This, together with the premature arrest of arteriogenic growth, as a result of the drop in FSS in the growing collateral, is a reason that collateral arteries cannot completely compensate the conductance of the artery they have replaced. Initially, during arteriogenesis, several collateral vessels are recruited and proliferate. However, as it is hemodynamically more efficient for fewer, larger arteries to conduct the blood than a greater number of smaller arteries, the smaller vessels regress later on, and those with the higher shear forces continue growing [17].

17. Hoefer, I. E., Piek, J. J., Pasterkamp, G. (2006) Pharmaceutical interventions to influence arteriogenesis: new concepts to treat ischemic heart disease. Curr. Med. Chem. 13, 979–987.

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Interestingly, Pipp et al.[44], demonstrated the importance of FSS in arteriogenesis by means of a porcine ischemic hindlimb model with extremely high levels of collateral flow and FSS. Normally, during the later phases of arteriogenesis, FSS decreases as the collateral diameter increases so that FSS normalizes. This drop in FSS acts as a signal to arrest proliferation and as a result, prevents further collateral growth before an optimal adaptation is reached. Pipp and colleagues [44] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic factor in collateral growth.

44. Pipp, F., et al., Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hindlimb. Arterioscler Thromb Vasc Biol, 2004. 24(9): p. 1664-8.

Interestingly, Pipp et al. [14] demonstrated the importance of FSS in arteriogenesis by means of a porcine ischemic hindlimb model with extremely high levels of collateral flow and FSS. Normally, during the later phases of arteriogenesis, FSS decreases as the collateral diameter increases so that FSS normalizes. This drop in FSS acts as a signal to arrest proliferation and as a result, prevents further collateral growth before an optimal adaptation

[Seite 1381]

is reached. Pipp and colleagues [14] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further, significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic power in collateral growth.


14. Pipp, F., Boehm, S., Cai, W. J., Adili, F., Ziegler, B., Karanovic, G., Ritter, R., Balzer, J., Scheler, C., Schaper, W., Schmitz-Rixen, T. (2004) Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. Arterioscler. Thromb. Vasc. Biol. 24, 1664–1668.

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Cardiovascular diseases are the number one cause of death globally[104]. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients [who do not benefit from these treatment options.]

104. Murray, C.J. and A.D. Lopez, Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet, 1997. 349(9063): p. 1436-42.

In fact, cardiovascular disorders are currently the leading cause of death globally [1]. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients who do not benefit from these treatment options.

1. World Health Organization (February 2007) Factsheet 317.

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Identification of markers of collateral growth could help in determining patient prognosis and predicting therapy response and maybe even lead to new, proarteriogenic therapies. Development of preclinical animal models is needed to test these methods, as extreme caution needs to be taken when extrapolating research in mice to the clinical setting. This will also enable further investigation of mechanisms, e.g., signaling molecules involved in collateral artery growth, extending our knowledge, and possibilities in therapeutic application. Future research will therefore involve investigation of the mechanisms behind the individual response to arteriogenesis. Identification of markers of collateral growth could help in determining patient prognosis and predicting therapy response and maybe even lead to new, proarteriogenic therapies.

[...] Development of preclinical animal models (preferably large animal models such as pigs) is needed to test these methods, as extreme caution needs to be taken when extrapolating research in mice to the clinical setting. This will also enable further investigation of mechanisms, e.g., signaling molecules involved in collateral artery growth, extending our knowledge, and possibilities in therapeutic application.

Future research will therefore involve investigation of the mechanisms behind the individual response to arteriogenesis and its relation to growth factor and cell therapy for the development of novel, therapeutic strategies.

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