Platelets as Potent Signaling Entities in Type 2 Diabetes Mellitus

T2DM has a multifactorial nature, and systemic inflammation, endothelial dysfunction, with resulting hypercoagulation and platelet dysfunction, are key disease elements. Increased circulating inflammatory markers are present in T2DM, and they originate from various sources, including the platelets themselves. Platelets have important cellular crosstalk functions in T2DM, and they become proinflammatory entities, driving inflammation in this condition. Platelets react to, for example, collagen and von Willebrand factor, and interfere with endothelial integrity. Focused platelet research may be an important avenue to pursue to find novel therapeutic targets or to be used as cellular activity sensors themselves. Type 2 diabetes mellitus (T2DM) is a multifactorial disease with a dysregulated circulating inflammatory molecule tendency. T2DM is closely associated with systemic inflammation, endothelial dysfunction, cardiovascular risk, and increased clotting susceptibility. Platelets have fundamental roles in the development and propagation of inflammation and cardiovascular risk. They signal through membrane receptors, resulting in (hyper)activation and release of inflammatory molecules from platelet compartments. This review highlights how circulating inflammatory molecules, acting as platelet receptor ligands, interact with platelets, causing platelets to be potent drivers of systemic inflammation. We conclude by suggesting that focused platelet research in T2DM is an important avenue to pursue to identify novel therapeutic targets, and that platelets could be used as cellular activity sensors themselves. Type 2 diabetes mellitus (T2DM) is a multifactorial disease with a dysregulated circulating inflammatory molecule tendency. T2DM is closely associated with systemic inflammation, endothelial dysfunction, cardiovascular risk, and increased clotting susceptibility. Platelets have fundamental roles in the development and propagation of inflammation and cardiovascular risk. They signal through membrane receptors, resulting in (hyper)activation and release of inflammatory molecules from platelet compartments. This review highlights how circulating inflammatory molecules, acting as platelet receptor ligands, interact with platelets, causing platelets to be potent drivers of systemic inflammation. We conclude by suggesting that focused platelet research in T2DM is an important avenue to pursue to identify novel therapeutic targets, and that platelets could be used as cellular activity sensors themselves.