Vascular morbidity and mortality are primary complications of diabetes and have been correlated with unregulated blood glucose control. Endothelial cells that line the vasculature are known to be dysfunctional in hyperglycemia (1). Furthermore, the high glucose environment promotes basement membrane protein glycation and enhanced cross-linking. This can increase matrix stiffness, decrease matrix degradation, and potentially alter the spatial distribution of cell-matrix binding sites.

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