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Insufficient neoangiogenesis is an integral component of loss of organ
function following chronic ischaemia or acute ischaemic injury due to
atherosclerotic plaque rupture and myocardial infarction. Therapeutic
angiogenesis promoting the growth of new vessels from existing vessel
wall cells, in conjunction with the recruitment of circulating
endothelial progenitor cells (EPCs), is therefore viewed as a highly
promising strategy to revascularise ischaemic tissues and thereby
improve functional recovery of injured organs. Identification of genes
involved in differentiation, homing and expansion of EPCs is of
paramount importance in developing ways to specifically target the
cells in sufficient numbers to ischaemic tissue.
A large body of evidence indicates that angiogenesis/vasculogenesis is
central in the repair process following tissue ischaemia. Therapeutic
neovascularisation is therefore considered as a very promising approach
to prevent the serious clinical consequences (heart failure, gangrene,
neuronal disability) of abnormal tissue remodelling in patients
suffering from cardiovascular ischaemic disease. Angiogenesis research
was recently revolutionized by the discovery that adult angiogenesis is
significantly bolstered by the recruitment of circulating endothelial
progenitor cells (EPCs) that functionally incorporate into forming
vessels.
The aim of this EVGN priority area is to identify novel genes, gene
products, or signalling pathways that are involved in, and could be
targets for, selective modulation of angiogenesis/vasculogenesis, and
define the most suitable therapeutic strategies for use in clinical
care
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