Mini-review explores cardiovascular complications in systemic lupus erythematosus, highlighting diagnostic and therapeutic strategies.
A BSTRACT Systemic lupus erythematosus (SLE) is a chronic autoimmune disease associated with a significantly increased risk of cardiovascular (CV) complications. The pathogenesis of them in SLE involves immune dysregulation, chronic inflammation, endothelial dysfunction, accelerated atherosclerosis, and programmed cell death pathways. Key contributors include autoantibodies (antibodies to double-stranded DNA and antiphospholipid antibodies), pro-inflammatory cytokines (interleukin-6 and interferon-alpha), oxidative stress, and impaired nitric oxide bioavailability. These factors promote endothelial injury, arterial stiffness, microvascular damage, and unstable plaque formation, leading to thrombotic events, myocardial infarction, and stroke. Emerging biomarkers such as microparticles and soluble RAGE may help assess CV risk. Management requires a multidisciplinary approach, targeting both traditional CV risk factors and SLE-specific mechanisms, including immunomodulatory therapies. This mini-review explores the underlying mechanisms of CV complications in SLE and discusses possible diagnostic and therapeutic strategies.
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Gizatullina et al. (2025) studied this question.
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