Improving the Outcome of Vein Grafts: Should Vascular Surgeons Turn Veins into Arteries?
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- Isaji Toshihiko
- The Department of Surgery and the Vascular Biology and Therapeutics Program, Yale University Department of Vascular Surgery, The University of Tokyo
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- Hashimoto Takuya
- The Department of Surgery and the Vascular Biology and Therapeutics Program, Yale University Department of Vascular Surgery, The University of Tokyo Department of Surgery, VA Connecticut Healthcare Systems
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- Yamamoto Kota
- Department of Vascular Surgery, The University of Tokyo
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- Santana Jeans M.
- The Department of Surgery and the Vascular Biology and Therapeutics Program, Yale University
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- Yatsula Bogdan
- The Department of Surgery and the Vascular Biology and Therapeutics Program, Yale University
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- Hu Haidi
- The Department of Surgery and the Vascular Biology and Therapeutics Program, Yale University
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- Bai Hualong
- The Department of Surgery and the Vascular Biology and Therapeutics Program, Yale University
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- Jianming Guo
- The Department of Surgery and the Vascular Biology and Therapeutics Program, Yale University
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- Kudze Tambudzai
- The Department of Surgery and the Vascular Biology and Therapeutics Program, Yale University
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- Nishibe Toshiya
- Department of Cardiovascular Surgery, Tokyo Medical University
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- Dardik Alan
- The Department of Surgery and the Vascular Biology and Therapeutics Program, Yale University Department of Surgery, VA Connecticut Healthcare Systems
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<p>Autogenous vein grafts remain the gold standard conduit for arterial bypass, particularly for the treatment of critical limb ischemia. Vein graft adaptation to the arterial environment, i.e., adequate dilation and wall thickening, contributes to the superior performance of vein grafts. However, abnormal venous wall remodeling with excessive neointimal hyperplasia commonly causes vein graft failure. Since the PREVENT trials failed to improve vein graft outcomes, new strategies focus on the adaptive response of the venous endothelial cells to the post-surgical arterial environment. Eph-B4, the determinant of venous endothelium during embryonic development, remains expressed and functional in adult venous tissue. After surgery, vein grafts lose their venous identity, with loss of Eph-B4 expression; however, arterial identity is not gained, consistent with loss of all vessel identity. In mouse vein grafts, stimulation of venous Eph-B4 signaling promotes retention of venous identity in endothelial cells and is associated with vein graft walls that are not thickened. Eph-B4 regulates downstream signaling pathways of relevance to vascular biology, including caveolin-1, Akt, and endothelial nitric oxide synthase (eNOS). Regulation of the Eph-B4 signaling pathway may be a novel therapeutic target to prevent vein graft failure.</p>
収録刊行物
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- Annals of Vascular Diseases
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Annals of Vascular Diseases 10 (1), 8-16, 2017
Annals of Vascular Diseases 編集委員会
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詳細情報 詳細情報について
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- CRID
- 1390282680252248960
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- NII論文ID
- 130005475941
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- ISSN
- 18816428
- 1881641X
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
- KAKEN
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- 抄録ライセンスフラグ
- 使用不可