Role of Platelet Hyperfunction in Pathogenesis of Atherosclerosis and Metabolic Syndrome
Valdas Banys
Summary
Coagulation and inflammatory processes are linked by common activation mechanisms, which are regul ated by common regulatory systems. Coagulation may trigger inflammatory reactions, while inflammation may activate coagulation. Plateles role in these processes is important in several aspects: receptor-dependent signal transduction mechanisms are activated; coagulation factors, cytokines, chemokines, adhesion receptors, growth factors are secreted; platelet microparticles are produced; platelets interact with other cells (leucocytes, monocytes, endothelial cells and endothelial progenitor cells). Entirety of these actions leads to progression of chronic inflammation, irreversible blood-vessel wall endothelial dysfunction - atherosclerosis. In this article major pathogenetic coherence between platelets, thrombosis and inflammation is reviewed, causes of increased platelets reactivity characteristic to atherosclerosis and metabolic syndrome are described: decreased nitric oxide production and decreased platelet sensitivity to prostaglandins, increased platelet dependent thrombin generation, increased expression of platelet surface receptors and adhesion molecules, increased production of free radicals, lipid peroxidation and oxidative stress. Some currently used (mean platelet volume, high density lipoprotein cholesterol) and potential (CD40L, CD36, monomeric CRP, RANTES, P selectin, platelet microparticles, peroxysome proliferator-activated receptors, different cytokines/chemo- kines and their receptors) laboratory markers of platelet hyperfunction are also presented.
Keywords: platelets, atherosclerosis, metabolic syndrome.
