Hypoxia mediated signalling in vein graft remodelling and failure

Research output: Contribution to journalMeeting abstractpeer-review


The use of autologous saphenous vein tissue is the first choice in bypass grafting. Although preferred over synthetic grafts, significant problems leading to occlusive blockage arise. Consequently over 30% of grafts require surgical revision within the first year of implantation. Autologous vein graft tissue undergoes adaptive remodelling to accommodate the change in haemodynamic environment, in effect undergoing "arterialisation". However, typically at anastomosis, remodelling results in excessive neointimal growth characterised by the proliferation and migration of vascular smooth muscle cells to the intimal causing expansion of the intimal layer. This hyperproliferative response ultimately develops to occlude blood flow. The excessive hyperproliferation is thought to be driven by desired remodelling, iatrogenic trauma and inflammation combined with ischaemia resulting in vein graft failure and clinical complications. Hypoxia as a consequence of global ischaemia is perhaps an important factor.
Hypoxia has been shown to modulate PLC-ɣ leading to the activation of PKC dependent- cell proliferation though mitogen activated protein kinases (MAPK) signalling pathways. Additionally, hypoxia is also responsible for the pro-mitogenic HIF-1α derived signalling pathway. The exact mechanisms of these pathways which result in the modification of cellular function including proliferation and apoptosis are not yet fully understood. Thus the project aims to investigate the role of hypoxia mediated signalling in vein graft remodelling.
Original languageEnglish
Issue numberS4
Publication statusPublished - 31 Dec 2014
EventBSCR: Cardiovascular Signalling in Health and Disease - University of Reading
Duration: 8 Sep 20159 Sep 2015


  • bypass surgery
  • grafts
  • hypoxia


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