Abstract
Reactive oxygen species (ROS) have physiological roles as second messengers, but can also exert detrimental modifications on DNA, proteins and lipids if resulting from enhanced generation or reduced antioxidant defense (oxidative stress). Venous thrombus (DVT) formation and resolution are influenced by ROS through modulation of the coagulation, fibrinolysis, proteolysis and the complement system, as well as the regulation of effector cells such as platelets, endothelial cells, erythrocytes, neutrophils, mast cells, monocytes and fibroblasts. Many conditions that carry an elevated risk of venous thrombosis, such as the Antiphospholipid Syndrome, have alterations in their redox homeostasis. Dietary and pharmacological antioxidants can modulate several important processes involved in DVT formation, but their overall effect is unknown and there are no recommendations regarding their use. The development of novel antioxidant treatments that aim to abrogate the formation of DVT or promote its resolution will depend on the identification of targets that enable ROS modulation confined to their site of interest in order to prevent off-target effects on physiological redox mechanisms. Subgroups of patients with increased systemic oxidative stress might benefit from unspecific antioxidant treatment, but more clinical studies are needed to bring clarity to this issue.
Highlights
Deep vein thrombosis (DVT) accounts for around 10 million cases of thrombosis per year and is the third most prevalent cardiovascular disease (CVD) after myocardial infarction and stroke
Neutrophils isolated from chronic granulomatous disease (CGD) patients produce 2- to 4-fold more IL-8 and show a sustained IL-8 mRNA response after fMLP stimulation compared with normal neutrophils, while normal neutrophils treated with an Reactive oxygen species (ROS) scavenger or NOX inhibitor have similar IL-8 responses to CGD neutrophils
It is not surprising that the molecules involved in leukocyte-attraction platelet-endothelial CAM-1 (PECAM-1), IL-8, Monocyte chemotactic protein-1 (MCP-1) have proangiogenic activity [128,132,145,148], all of which we have described as being modulated by ROS
Summary
Deep vein thrombosis (DVT) accounts for around 10 million cases of thrombosis per year and is the third most prevalent cardiovascular disease (CVD) after myocardial infarction and stroke. Venous reflux in DVT-damaged veins (post-thrombotic syndrome) is, the main driver of DVT-associated morbidity, causing pain, swelling and, when severe, chronic skin ulceration. Anticoagulation is the most common approach taken when treating DVT, but these drugs inhibit thrombus propagation, they are associated with an increased risk of pathological bleeding such as stroke. 2. TVheenoduesvTelhorpommebnuts oFforamvaetnioonus thrombus requires activation of the endothelium, platelets and sterile inflammation (involving neutrophils, mast cells and monocytes), stimulated by the interaction betweenThaet ldeeavsetltowpmo oenf tVoirfcahovwen’osutrsiathdroomf fbaucstorresq:urierdesuaccetdivbaltoioondoflfotwhe; eennddootthheelliiuaml d, ipsltautrebleatns caen;dand theshteyrpileericnoflaagmumlaabtiilointy(ionfvbollovoindg. Of the coagulation system and platelet aggregation; mast cell degranulation and tissue factor (TF) production within the vein wall. Neutrophil extracellular traps (NETs) provide an additional scaffold and contribute to further oxidative stress and thrombus formation
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