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Vascular damage in systemic lupus erythematosus
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Vascular damage in systemic lupus erythematosus
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Vascular damage in systemic lupus erythematosus
Vascular damage in systemic lupus erythematosus
Journal Article

Vascular damage in systemic lupus erythematosus

2024
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Overview
Vascular disease is a major cause of morbidity and mortality in patients with systemic autoimmune diseases, particularly systemic lupus erythematosus (SLE). Although comorbid cardiovascular risk factors are frequently present in patients with SLE, they do not explain the high burden of premature vascular disease. Profound innate and adaptive immune dysregulation seems to be the primary driver of accelerated vascular damage in SLE. In particular, evidence suggests that dysregulation of type 1 interferon (IFN-I) and aberrant neutrophils have key roles in the pathogenesis of vascular damage. IFN-I promotes endothelial dysfunction directly via effects on endothelial cells and indirectly via priming of immune cells that contribute to vascular damage. SLE neutrophils are vasculopathic in part because of their increased ability to form immunostimulatory neutrophil extracellular traps. Despite improvements in clinical care, cardiovascular disease remains the leading cause of mortality among patients with SLE, and treatments that improve vascular outcomes are urgently needed. Improved understanding of the mechanisms of vascular injury in inflammatory conditions such as SLE could also have implications for common cardiovascular diseases, such as atherosclerosis and hypertension, and may ultimately lead to personalized therapeutic approaches to the prevention and treatment of this potentially fatal complication.Here, the authors review traditional and disease-specific risk factors for vascular damage and the cellular and molecular mechanisms that drive vascular injury in systemic lupus erythematosus. They also discuss cardiovascular risk assessment, primary prevention strategies and current and future treatment approaches to cardiovascular disease in systemic lupus erythematosus.
Publisher
Nature Publishing Group