Inflammation, platelets and diabetes

F. Santilli, P. Simeone, R. Liani
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Abstract

Type 2 diabetes is a key player in atherothrombosis. Inflammation participates in metabolic homeostasis interacting with adipose tissue-specific macrophages. Platelets appear as addresses and players carrying and transducing metabolic derangement into vascular injury. AGE-RAGE pathway is recognized as the driver of metabolic memory. Human platelets have insulin receptors that participate in the regulation of platelet function and platelets are potential sites of insulin resistance. The present mini-review addresses key pathophysiological aspects including i) the role of inflammation in the pathogenesis of diabetes; ii) platelets as inflammatory cells; iii) the involvement on inflammation in the interindividual variability in aspirin response. Taken together, these aspects may contribute to expand knowledge about the link between the extent of inflammation, platelet activation and turnover, and interindividual variability in the development of atherothrombosis and its prevention, in a view of precision medicine.
炎症,血小板和糖尿病
2型糖尿病是动脉粥样硬化血栓形成的关键因素。炎症参与代谢稳态与脂肪组织特异性巨噬细胞相互作用。血小板作为地址和玩家出现,携带和转导代谢紊乱进入血管损伤。AGE-RAGE通路被认为是代谢记忆的驱动因素。人类血小板有胰岛素受体参与血小板功能的调节,血小板是胰岛素抵抗的潜在位点。本综述涉及的主要病理生理方面包括:1)炎症在糖尿病发病机制中的作用;Ii)血小板作为炎症细胞;Iii)阿司匹林反应的个体差异与炎症的关系。综上所述,从精准医学的角度来看,这些方面可能有助于扩大对炎症程度、血小板活化和周转、动脉粥样硬化血栓形成及其预防的个体差异之间的联系的认识。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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