糖尿病患者血小板的过度活跃和促炎功能

IF 3.1 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY Frontiers in bioscience (Landmark edition) Pub Date : 2025-01-08 DOI:10.31083/FBL26190
Jordan Greaves, Giordano Pula
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引用次数: 0

摘要

心血管并发症夺去了高达70%的糖尿病患者的生命。糖尿病增加心血管风险的机制仍有待充分了解和成功解决。尽管如此,科学文献中越来越多的证据表明血小板参与糖尿病心血管并发症。多篇报道描述了糖尿病中血小板的高活性及其参与炎症反应。了解血小板对糖尿病心血管病理的作用机制将有助于开发能够降低这些患者心血管风险的靶向治疗策略。在这篇文献综述中,我们总结了我们目前对导致血小板对糖尿病心血管风险贡献的分子机制的理解。导致血栓形成和参与炎症过程的血小板止血活性都受到糖尿病相关生化条件的刺激。我们还提供了糖尿病如何影响现有血栓治疗效果的证据,反之,降糖药如何影响血小板功能和止血/血栓平衡。综上所述,越来越多的证据表明血小板在糖尿病进展中的不同和意想不到的作用,为设计针对血小板的心血管药物、血小板的促炎活性及其在糖尿病中的激活机制提供了强有力的理论依据。总之,这篇文章提供了糖尿病患者血小板病理生理改变的重要最新概述,这需要考虑到有效管理心血管健康的疾病。
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Hyperactivity and Pro-inflammatory Functions of Platelets in Diabetes.

Cardiovascular complications claim the lives of up to 70% of patients with diabetes mellitus (DM). The mechanisms increasing cardiovascular risk in DM remain to be fully understood and successfully addressed. Nonetheless, there is increasing evidence in the scientific literature of the participation of platelets in the cardiovascular complications of DM. Multiple reports describe the hyperactivity of platelets in DM and their participation in inflammatory responses. The understanding of the mechanisms underlying the contribution of platelets to cardiovascular pathologies in DM will help the development of targeted therapeutic strategies able to reduce cardiovascular risk in these patients. In this literature review, we summarise our current understanding of the molecular mechanisms leading to the contribution of platelets to cardiovascular risk in DM. Both platelet haemostatic activity leading to thrombus formation and their participation to inflammatory processes are stimulated by the biochemical conditions associated with DM. We also present evidence on how DM affect the efficacy of existing therapeutic treatments for thrombosis and, by converse, how antidiabetic drugs may affect platelet function and the haemostasis/thrombosis balance. Taken together, the growing evidence of the different and unexpected roles of platelets in the progression of DM provides a strong rationale for the design of cardiovascular drugs targeting specifically platelets, their pro-inflammatory activity and their activation mechanisms in this disease. Overall, this article provides an important up-to-date overview of the pathophysiological alterations of platelets in DM, which need to be taken into account for the effective management of cardiovascular health in this disease.

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