Atherosclerosis is one of the main complications of diabetes involving multiple causative factors. Dysfunction of the vascular endothelium is a hallmark of most conditions that are associated with both diabetes and atherosclerosis. Although the pathological link between diabetes and atherosclerosis is well-established, better comprehension of the underlying mechanisms is of utmost importance to identify novel potential molecular targets. It is difficult to separate the effects of hyperglycaemia from those of other atherogenic factors: recent evidence shows that they share many common mechanisms, such as endothelial activation and inflammation, mitochondrial oxidative stress, changes in extracellular matrix components and disruption of cellular defence systems. The plausible hypothesis of the ‘common soil’ between diabetes and atherosclerosis seems to be born from a unique ‘ancestor’: the nuclear factor κB, a transcription factor able to guide multiple molecular processes. It seems that this master regulator triggers either some hyperglycaemia-induced effects on the endothelial function, or the expression of certain microRNAs (in particular miR-126, -21 and miR-146a-5p) involved in favouring atherosclerosis. Here, we review the latest evidence and proposed mechanisms, aiming to understand the link between diabetes and atherosclerosis.
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