Angiogenesis, the extension of existing vasculature by sprouting of capillaries from post-capillary venules, is a complex process involving increases in vascular permeability, matrix degradation, and migration and proliferation of endothelial cells. Formation of new blood vessels is a key process within diseased vascular tissues, where it may sustain or destabilise atherosclerotic plaques [1]; intimal neo-vascularisation increases as arterial walls increase in thickness and complexity, with the microvessel density greatest in lesions with marked macrophage and lipid infiltration, and focused at macrophage-rich and rupture-prone ‘shoulders’ of vulnerable plaques [2]. Angiogenesis is also an integral feature of adipogenesis, as continuous remodelling of the vascular network is required to sustain adipocyte hyperplasia and hypertrophy [3]. ‘Classical’ pro-angiogenic factors, such as members of the vascular endothelial growth factor (VEGF) family, are abundantly expressed by cells within the arterial wall, and within human atherosclerotic lesions. However, novel bioactive ‘adipokines’ derived from adipose and other tissues via the systemic circulation, have recently been identified which possess pro-angiogenic actions, including leptin, adiponectin, visfatin, apelin and resistin [3], [4] and [5], leading to the suggestion that increased neovascularisation may be one mechanism contributing to the established link between obesity and cardiovascular disease [6]. Equally, these factors may mediate the developing neovasculature required to support adipose tissue expansion [3].