Figure 2.

Metabolic dysregulation in T2DM will contribute to greater platelet hyperreactivity. Dysregulated metabolic conditions in patients with T2DM will result in: (1) lower production of NO and PGI2; (2) reduced inhibition of the P2Y12 pathway; (3) increased oxidative stress and intracellular Ca²⁺ signaling activate the PKC pathway; (4) decreased production of antioxidants; (5) increased protein glycation on the platelet surface; (6) enhanced surface expression of glycoproteins, such as GPIb and GPIIb/IIIa. Together, these factors contribute to a prothrombotic environment, thus promoting the development of vascular occlusion and atherothrombosis in T2DM.