Diabetes mellitus exposes endothelial cells (ECs) to a chronic hyperglycaemic milieu, leading to dysfunction of the vascular endothelium. The resulting microvasculature rarefaction leads to tissue hypoperfusion and propagates the occurrence of ischaemic events, such as critical limb ischaemia and ischaemic heart disease. Moreover, hyperglycaemia impairs the angiogenic potential of ECs thereby compromising post-ischaemic reparative neovascularisation. N6-methyladenosine (m6A) is emerging as a new layer for fine-tuning gene expression. The functional importance of m6A has been revealed in a plethora of fundamental bioprocesses, while its dysregulation has been linked to several diseases including diabetes. However, our understanding of the precise roles of m6A in the cardiovascular system is still in its infancy and its significance in diabetes associated complications of the vasculature remains completely unexplored. This study elucidates a novel role for METTL3, the primary m6A methylase, in the regulation of angiogenesis. Loss and gain of function studies reveal METTL3 to be crucial in the modulation of EC processes that are conducive to angiogenesis in vitro and in vivo. Mechanistically, METTL3 modulates angiogenesis by mediating the endothelial bioprocessing of the angiogenic miRNAs let-7e and the miR-17-92 cluster. Expressional analysis revealed a dysregulation of m6A and METTL3 in human ECs exposed to diabetic and ischaemic mimicking conditions, ECs derived from a murine model of diabetic LI and in left ventricular tissue and ECs isolated from diabetic mouse hearts. The therapeutic potential of endothelial METTL3 was demonstrated using murine models of diabetic limb ischaemia and myocardial infarction. Here, the adenovirus mediated overexpression of METTL3 in ischaemic limb muscles improved post-ischaemic muscular neovascularisation. Additionally, infarcted hearts treated with Ad.METTL3 showed an increase in arteriole and capillary densities while exhibiting improved contractile function. Thus, the findings in this thesis suggest that the modulation of METTL3 could represent novel therapeutic target for ischaemic complications in diabetic patients.