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.

血管疾病是系统性自身免疫性疾病，特别是系统性红斑狼疮（SLE）患者发病和死亡的主要原因。尽管 SLE 患者经常存在合并心血管危险因素，但它们并不能解释过早发生血管疾病的高负担。严重的先天性和适应性免疫失调似乎是 SLE 血管损伤加速的主要驱动因素。特别是，有证据表明 1 型干扰素 (IFN-I) 和异常中性粒细胞的失调在血管损伤的发病机制中发挥着关键作用。IFN-I通过对内皮细胞的作用直接促进内皮功能障碍，并通过引发导致血管损伤的免疫细胞间接促进内皮功能障碍。SLE 中性粒细胞出现血管病变的部分原因是它们形成免疫刺激性中性粒细胞胞外陷阱的能力增强。尽管临床护理有所改善，心血管疾病仍然是 SLE 患者死亡的主要原因，迫切需要改善血管结局的治疗。更好地了解系统性红斑狼疮等炎症性疾病中血管损伤的机制也可能对动脉粥样硬化和高血压等常见心血管疾病产生影响，并可能最终导致预防和治疗这种潜在致命并发症的个性化治疗方法。