Leeds Institute of Cardiovascular and Metabolic Medicine, Faculty of Medicine and Health, University of Leeds, Leeds LS2 9JT, UK.
Int J Mol Sci. 2022 Apr 29;23(9):4973. doi: 10.3390/ijms23094973.
Cardiovascular complications remain the leading cause of morbidity and mortality in individuals with diabetes, driven by interlinked metabolic, inflammatory, and thrombotic changes. Hyperglycaemia, insulin resistance/deficiency, dyslipidaemia, and associated oxidative stress have been linked to abnormal platelet function leading to hyperactivity, and thus increasing vascular thrombotic risk. However, emerging evidence suggests platelets also contribute to low-grade inflammation and additionally possess the ability to interact with circulating immune cells, further driving vascular thrombo-inflammatory pathways. This narrative review highlights the role of platelets in inflammatory and immune processes beyond typical thrombotic effects and the impact these mechanisms have on cardiovascular disease in diabetes. We discuss pathways for platelet-induced inflammation and how platelet reprogramming in diabetes contributes to the high cardiovascular risk that characterises this population. Fully understanding the mechanistic pathways for platelet-induced vascular pathology will allow for the development of more effective management strategies that deal with the causes rather than the consequences of platelet function abnormalities in diabetes.
心血管并发症仍然是糖尿病患者发病率和死亡率的主要原因，其驱动因素是相互关联的代谢、炎症和血栓形成变化。高血糖、胰岛素抵抗/缺乏、血脂异常和相关的氧化应激与异常的血小板功能有关，导致过度活跃，从而增加血管血栓形成风险。然而，新出现的证据表明，血小板也有助于低度炎症，并且还具有与循环免疫细胞相互作用的能力，进一步推动血管血栓炎症途径。本综述强调了血小板在炎症和免疫过程中的作用超出了典型的血栓形成效应，以及这些机制对糖尿病心血管疾病的影响。我们讨论了血小板诱导炎症的途径，以及糖尿病中血小板重编程如何导致该人群特有的高心血管风险。充分了解血小板诱导血管病理的机制途径将有助于制定更有效的管理策略，这些策略针对的是糖尿病中血小板功能异常的原因，而不仅仅是后果。
