Abstract
Proliferation and migration of smooth muscle cells and the resultant intimal hyperplasia cause coronary artery bypass graft failure. Both internal mammary artery and saphenous vein are the most commonly used bypass conduits. Although an internal mammary artery graft is immune to restenosis, a saphenous vein graft is prone to develop restenosis. We found significantly higher activity of phosphatase and tensin homolog (PTEN) in the smooth muscle cells of the internal mammary artery than in the saphenous vein. In this article, we critically review the pathophysiology of vein-graft failure with detailed discussion of the involvement of various factors, including PTEN, matrix metalloproteinases, and tissue inhibitor of metalloproteinases, in uncontrolled proliferation and migration of smooth muscle cells towards the lumen, and invasion of the graft conduit. We identified potential target sites that could be useful in preventing and (or) reversing unwanted consequences following coronary artery bypass graft using saphenous vein.
| Original language | English |
|---|---|
| Pages (from-to) | 531-545 |
| Number of pages | 15 |
| Journal | Canadian Journal of Physiology and Pharmacology |
| Volume | 92 |
| Issue number | 7 |
| DOIs | |
| State | Published - 2014 |
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All Science Journal Classification (ASJC) codes
- Physiology
- Physiology (medical)
- Pharmacology
- Medicine(all)
Cite this
Coronary artery bypass graft : Why is the saphenous vein prone to intimal hyperplasia?1. / Sur, Swastika; Sugimoto, Jeffrey T.; Agrawal, Devendra K.
In: Canadian Journal of Physiology and Pharmacology, Vol. 92, No. 7, 2014, p. 531-545.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Coronary artery bypass graft
T2 - Why is the saphenous vein prone to intimal hyperplasia?1
AU - Sur, Swastika
AU - Sugimoto, Jeffrey T.
AU - Agrawal, Devendra K.
PY - 2014
Y1 - 2014
N2 - Proliferation and migration of smooth muscle cells and the resultant intimal hyperplasia cause coronary artery bypass graft failure. Both internal mammary artery and saphenous vein are the most commonly used bypass conduits. Although an internal mammary artery graft is immune to restenosis, a saphenous vein graft is prone to develop restenosis. We found significantly higher activity of phosphatase and tensin homolog (PTEN) in the smooth muscle cells of the internal mammary artery than in the saphenous vein. In this article, we critically review the pathophysiology of vein-graft failure with detailed discussion of the involvement of various factors, including PTEN, matrix metalloproteinases, and tissue inhibitor of metalloproteinases, in uncontrolled proliferation and migration of smooth muscle cells towards the lumen, and invasion of the graft conduit. We identified potential target sites that could be useful in preventing and (or) reversing unwanted consequences following coronary artery bypass graft using saphenous vein.
AB - Proliferation and migration of smooth muscle cells and the resultant intimal hyperplasia cause coronary artery bypass graft failure. Both internal mammary artery and saphenous vein are the most commonly used bypass conduits. Although an internal mammary artery graft is immune to restenosis, a saphenous vein graft is prone to develop restenosis. We found significantly higher activity of phosphatase and tensin homolog (PTEN) in the smooth muscle cells of the internal mammary artery than in the saphenous vein. In this article, we critically review the pathophysiology of vein-graft failure with detailed discussion of the involvement of various factors, including PTEN, matrix metalloproteinases, and tissue inhibitor of metalloproteinases, in uncontrolled proliferation and migration of smooth muscle cells towards the lumen, and invasion of the graft conduit. We identified potential target sites that could be useful in preventing and (or) reversing unwanted consequences following coronary artery bypass graft using saphenous vein.
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UR - http://www.scopus.com/inward/citedby.url?scp=84903272683&partnerID=8YFLogxK
U2 - 10.1139/cjpp-2013-0445
DO - 10.1139/cjpp-2013-0445
M3 - Article
VL - 92
SP - 531
EP - 545
JO - Canadian Journal of Physiology and Pharmacology
JF - Canadian Journal of Physiology and Pharmacology
SN - 0008-4212
IS - 7
ER -