Key result
Oxidative stress drives antiphospholipid antibody production and promotes atherothrombotic complications in antiphospholipid syndrome.
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Review highlights oxidative stress mechanisms driving atherothrombosis in antiphospholipid syndrome, suggesting novel antioxidant therapeutic strategies.
Atherothrombosis is a frequent complication of the clinical history of patients with antiphospholipid syndrome (APS). Both atherothrombosis and APS are characterized by increased oxidative stress. Oxidative modifications are implicated in the formation of antiphospholipid antibodies, which in turn may favour the oxidative imbalance by increasing the production of reactive oxidant species (ROS) or by a direct interaction with pro-oxidant/antioxidant enzymes. As a result of these processes, APS patients suffer from an oxidative imbalance that may contribute to the progression of the atherosclerotic process and to the onset of ischemic thrombotic complications. The aim of this review is to describe mechanisms implicated in the formation of ROS in APS patients and their involvement in the atherothrombotic process. We also provide an overview of potential therapeutic approaches to blunt oxidative stress and to prevent atherothrombotic complications in these patients.
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Nocella et al. (2021) conducted a review in Antiphospholipid syndrome (APS) and atherothrombosis. Oxidative stress and reactive oxidant species (ROS) formation was evaluated on Atherothrombotic complications and atherosclerotic progression. Oxidative stress and reactive oxidant species formation in antiphospholipid syndrome promote antiphospholipid antibody generation and contribute to atherothrombotic complications.
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