Proton Pump Inhibitors (PPIs) are inhibitors or risk factor for Atrial Fibrillation?

Glucose metabolism disorders are significant risk factors for accelerated atherosclerosis, but the exact pathogenesis of this impact and possible co-factors are not precisely known. On the other hand, only two thirds of all atherosclerosis cases are linked to so-called "classic" risk factors, and numerous studies are conducted to recognize those non-classic risk factors, among which homocysteine and adhesive molecules are the most often mentioned. Recently, the class B scavenger receptor CD36 has become an object of interest. Receptor CD36 is a membrane glycoprotein found on the surface of many cells, such as endothelial cells, cardiomyocytes, dendritic cells, platelets, monocytes, and macrophages. Ligands for receptor CD36 are oxidized LDL particles, long-chain fatty acids, collagens, thrombospondin I, apoptotic cells, and phospholipids. Receptor CD36 plays an important role in various processes, e.g. inner immune system response, apoptotic and necrotic cells removal, transport of fatty acids, and inhibition of neoplastic angiogenesis. Scavenging oxidized LDL particles is one of its most important functions. The most recent studies put forward the participation of receptor CD36 in atherogenesis. Additionally, increased CD36 expression has been described in diabetes mellitus and insulin resistance and in the pathogenesis of diabetic macro- and microangiopathy. Confounding data regarding human hereditary receptor CD36 deficiency as well as still unknown interactions between antidiabetic drugs and CD36 expression suggest the necessity for further studies on the participation of receptor CD36 in the atherogenesis linked with glucometabolic disorders and in the development of diabetes mellitus complications.