Arterialization of a vein graft promotes cell cycle progression through Akt and p38 mitogen-activated protein kinase pathways: Impact of the preparation procedure

Chung, Angie Y.; Wong, Jerry; Luo, Honglin; Hsiang, York; Breemen, Cornelis van; Okon, Elena B.

doi:10.1016/s0828-282x(07)70886-3

Cited by 8 publications

(2 citation statements)

References 37 publications

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“…Topical MAPK inhibitors significantly suppressed graft disease in a rabbit inter-positional model of vein grafting [78] , although not cell-specific, this provides further evidence for the role of MAPK in vein graft failure. Moreover, pharmacological vasorelaxation suppressed p38 activity and restricted the activation of proliferation and cell cycle progression in the porcine carotid jugular interposition graft [79] . Further evidence for the inhibition of inflammatory processes in vein graft disease is scarce.…”

Section: Intimal Hyperplasia and The Endotheliummentioning

confidence: 94%

Activation and inflammation of the venous endothelium in vein graft disease

et al. 2017

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The long saphenous vein is the most commonly used conduit in coronary artery bypass graft (CABG) surgery when bypassing multiple diseased arteries; however, its use is complicated by the development of vascular inflammation, intimal hyperplasia and accelerated atherosclerosis leading to compromised graft efficacy. Despite refinement of surgical techniques to improve graft patency, late vein graft failure remains a significant problem. Moreover, there is a lack of pharmacological interventions proven to be effective in the treatment of late vein graft failure. A greater understanding of the molecular nature of the disease and the interactions between endothelial and smooth muscle cells as a result of alterations in local haemodynamics may assist with designing future beneficial pharmacological interventions. Venous endothelial cells (ECs) are physiologically adapted to chronic low shear stress; however, once the graft is implanted into the arterial circulation, they become suddenly exposed to acute high levels of shear stress. A small number of in vitro and ex vivo studies have demonstrated that acute high shear stress is associated with the activation of a pro-inflammatory profile in saphenous vein ECs, which may be mediated by mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) signalling pathways. The impact of acute changes in shear stress on venous ECs and the role of ECs in the development of intimal hyperplasia remains incomplete and is the subject of this review.

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Section: Intimal Hyperplasia and The Endotheliummentioning

confidence: 94%

Activation and inflammation of the venous endothelium in vein graft disease

et al. 2017

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“…61 In the porcine carotid jugular interposition graft, it has been suggested that the use of pharmacological vasorelaxation (PV) suppresses p38 activity and restricts the activation of proliferation and cell cycle progression. 62 NF-κB regulates the leukocyte adhesion cascade (e.g. VCAM-1) and can contribute to sub-endothelial transmigration and the release of pro-inflammatory mediators.…”

Section: Glucocorticoids and Vein Graft Disease (Intimal Hyperplasia)mentioning

confidence: 99%

Glucocorticoids in adult cardiac surgery; old drugs revisited

Zakkar

Kanagasabay

2013

Perfusion

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Glucocorticoids can play a pivotal role in modulating different immune responses. The role of glucocorticoids in cardiac surgery is still controversial as many surgeons are concerned about the potential side effects.In this review, we looked at the role of glucocorticoid administration in modulating postoperative inflammatory responses, atrial fibrillation (AF) and intimal hyperplasia and whether glucocorticoid use is associated with a significant increase in undesirable postoperative complication.

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