Abstract
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.
Highlights
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are highly reactive molecules, generated in response to both endogenous and exogenous stimuli
Both NOX1 and NOX2 significantly contribute to ROS production, and they are considered responsible for the regulation of platelet responsiveness [39]
Magwenzi and colleagues have recently demonstrated that oxidized low-density lipoprotein (ox-LDL)/CD36 binding induced the activation of a tyrosine kinase and PKC-signaling that led to NOX2-mediated ROS generation
Summary
Reactive oxygen species (ROS) and reactive nitrogen species (RNS) are highly reactive molecules, generated in response to both endogenous and exogenous stimuli. Plateletsthrombus are anucleated cells derived from megakaryocytes which play a crucial role Human thrombopoiesis is finely tuned, since the number and function of circulating platelets are in hemostasis, thrombus formation, atherosclerosis, inflammation and immune response [15,16,17]. ROS, Despite changes in redox occur physiologically during production platelet activation, the onset of in turn, alters mitochondria function and boosts platelet activation in an auto-amplifying loop [34]. Oxidative stress has been described in several disorders including atherosclerosis, diabetes mellitus, hypertension, obesity, and cancer [35,36] In these pathological settings, oxidative stress is the secondary outcome of the diseases; the increased oxidative burden in the circulation exposes platelets to a pro-activatory milieu, responsible for platelet pro-adhesive and pro-aggregatory phenotype, which in turn lead to thromboembolic propensity, a common characteristic of all these diseases. This process generates a vicious circle capable to affect other cell types, eventually contributing to diseases progression and complications
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