Abstract
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.
Highlights
IntroductionIn the early 1980s, the term antiphospholipid syndrome (APS) was coined to describe an autoimmune, multisystemic disorder characterized clinically by autoantibody-induced thrombophilia [1]
As nicotinamide adenine dinucleotide phosphate (NADPH) oxidase is the main source of reactive oxidant species (ROS) [57], the results suggest that NADPH oxidase-mediated oxidative stress leads to endothelial cell injury in antiphospholipid syndrome (APS)
Oxidative stress is directly involved in the pathogenesis of atherothrombosis in APS
Summary
In the early 1980s, the term antiphospholipid syndrome (APS) was coined to describe an autoimmune, multisystemic disorder characterized clinically by autoantibody-induced thrombophilia [1]. APS is considered an autoimmune, thrombo-inflammatory disease characterized by vascular thrombosis in the setting of one or more antiphospholipid antibodies (aPLs) such as lupus anticoagulant (AL), anticardiolipin antibodies (aCL) and anti-β2-glycoprotein antibodies (aβ2GPI) [2]. APS regularly manifests with other morbid features including thrombocytopenia, cardiac dysfunction [3], accelerated atherosclerosis, nephropathy, movement disorders, and cognitive decline [4,5]. This heterogeneous clinical presentation reflects the complex pathogenesis of APS, reinforc- 4.0/).
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