Correspondingly, a previous study showed that 400 nM LY-333531 (resembling an all-PKC isoforms inhibiting concentration) does not further prevent hyperglycaemia-induced monocyte attachment to human ECs when compared with 10 nM LY-33351 (a PKC-β specific inhibiting concentration) [29], further showing the dominant role of PKC-β activation in endothelial dysfunction. Here, PRKCB is linked to endothelial dysfunction.