The latest in systemic lupus erythematosus-accelerated atherosclerosis: related mechanisms inform assessment and therapy.
The latest in systemic lupus erythematosus-accelerated atherosclerosis: related mechanisms inform assessment and therapy.
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系统性红斑狼疮加速动脉粥样硬化的最新进展：相关机制为评估和治疗提供信息。
DOI：
10.1097/bor.0000000000000773
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发表时间：
2021-03-01
影响因子：
5.1
通讯作者：
Major AS
中科院分区：
文献类型：
--
作者：
Appleton BD;Major AS
加速动脉粥样硬化是系统性红斑狼疮（SLE）患者的重要合并症和主要死亡原因。现在很明显，sled加速动脉粥样硬化不仅仅是由传统的心血管危险因素驱动的，这增加了疾病表征和机制理解的复杂性。在这篇综述中，我们将总结一些关于sl加速动脉粥样硬化的评价、治疗和机制的新见解。最近的工作强调了将炎症生物标志物纳入心血管疾病（CVD）风险评估的必要性。对于SLE患者尤其如此，其免疫功能障碍机制可能驱动CVD进展。有新的证据表明，常用的SLE治疗药物会阻碍动脉粥样硬化的发展。这种效果是通过减少sled相关炎症和直接改善动脉粥样硬化措施来实现的，强调了这两种情况的相互作用机制。sle加速的动脉粥样硬化很可能是慢性自身免疫性炎症的结果。因此，动脉粥样硬化的有效管理需要评估SLE疾病活动性以及传统的心血管危险因素。这支持了为什么许多传统上用于控制SLE的治疗方法也可以调节动脉粥样硬化的发展。更深入地了解这种情况的潜在机制将有助于开发更有针对性的治疗方法，并改善SLE患者的预后。
Accelerated atherosclerosis is a significant co-morbidity and the leading cause of death for patients with systemic lupus erythematosus (SLE). It is now apparent that SLE-accelerated atherosclerosis is not driven solely by traditional cardiovascular risk factors, adding complexity to disease characterization and mechanistic understanding. In this review, we will summarize new insights into SLE-accelerated atherosclerosis evaluation, treatment, and mechanism. Recent work highlights the need to incorporate inflammatory biomarkers into cardiovascular disease (CVD) risk assessments. This is especially true for SLE patients, where mechanisms of immune dysfunction likely drive CVD progression. There is new evidence that commonly prescribed SLE therapeutics hinder atherosclerosis development. This effect is achieved both by reducing SLE-associated inflammation and by directly improving measures of atherosclerosis, emphasizing the interconnected mechanisms of the two conditions. SLE-accelerated atherosclerosis is most likely the consequence of chronic autoimmune inflammation. Therefore, diligent management of atherosclerosis requires assessment of SLE disease activity as well as traditional cardiovascular risk factors. This supports why many of the therapeutics classically used to control SLE also modulate atherosclerosis development. Greater understanding of the mechanisms underlying this condition will allow for the development of more targeted therapeutics and improved outcomes for SLE patients.