Fig. 4
(Adapted from Kakouros et al. [16])
Mechanisms responsible for platelet hyperreactivity in T2DM patient: Elevated cAMP levels leading to platelet inhibition via cAMP-dependent protein kinase (PKA), which disrupt signaling via receptor activation, thromboxane A2 production, MAPK pathway, activation of PKC. The transmembrane G-protein associated receptors involved are prostaglandin, P2Y, P2X, TR, and TP. Both TR and TP present novel drug targets. Antiplatelet drugs are shown in red. NO nitric oxide, AGE advanced glycation end products, RAGE AGE receptors, PKA/B/C protein kinase A/B/C, TK tyrosine kinase, PI-3 phosphoinositol-3 kinase, MAPK p38 mitogen-activated protein kinase, GC guanylate cyclase, PAR-1 protease activated receptor, TR thrombin receptor, TPα thromboxane receptor, TRA thrombin receptor antagonist, TPRA thromboxane receptor antagonist, ASA acetylsalicylic acid (aspirin)