Department of Medicine and Surgery, University of Parma, 43126 Parma, Italy.
School of Pharmacy and Biomedical Sciences, Faculty of Health Sciences, Curtin University, Bentley, Perth, WA 6102, Australia.
Int J Mol Sci. 2020 Jul 9;21(14):4866. doi: 10.3390/ijms21144866.
Reactive oxygen species (ROS) and mitochondria play a pivotal role in regulating platelet functions. Platelet activation determines a drastic change in redox balance and in platelet metabolism. Indeed, several signaling pathways have been demonstrated to induce ROS production by NAPDH oxidase (NOX) and mitochondria, upon platelet activation. Platelet-derived ROS, in turn, boost further ROS production and consequent platelet activation, adhesion and recruitment in an auto-amplifying loop. This vicious circle results in a platelet procoagulant phenotype and apoptosis, both accounting for the high thrombotic risk in oxidative stress-related diseases. This review sought to elucidate molecular mechanisms underlying ROS production upon platelet activation and the effects of an altered redox balance on platelet function, focusing on the main advances that have been made in platelet redox biology. Furthermore, given the increasing interest in this field, we also describe the up-to-date methods for detecting platelets, ROS and the platelet bioenergetic profile, which have been proposed as potential disease biomarkers.
活性氧 (ROS) 和线粒体在调节血小板功能方面发挥着关键作用。血小板激活决定了氧化还原平衡和血小板代谢的剧烈变化。事实上,已经证实了几种信号通路可以通过 NADPH 氧化酶 (NOX) 和线粒体诱导 ROS 的产生,进而促进进一步的 ROS 产生和随后的血小板激活、黏附和募集,形成自我放大循环。这种恶性循环导致血小板促凝表型和细胞凋亡,这两者都与氧化应激相关疾病中的高血栓形成风险有关。本综述旨在阐明血小板激活时 ROS 产生的分子机制以及氧化还原平衡改变对血小板功能的影响,重点介绍血小板氧化还原生物学方面的主要进展。此外,鉴于人们对该领域的兴趣日益增加,我们还描述了目前用于检测血小板、ROS 和血小板生物能量谱的方法,这些方法被认为是潜在的疾病生物标志物。