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The link between dysregulated immunometabolism and vascular damage: Implications for the development of atherosclerosis in SLE and other rheumatic diseases.
The Journal of Rheumatology ( IF 3.9 ) Pub Date : 2024-01-15 , DOI: 10.3899/jrheum.2023-0833
Anjali S. Yennemadi , Natasha Jordan , Sophie Diong , Joseph Keane , Gina Leisching

A bimodal pattern of mortality in Systemic Lupus Erythematosus (SLE) exists. Early-stage deaths are predominantly caused by infection, while later-stage deaths are caused mainly by atherosclerotic disease. Further, while SLE-related mortality has reduced considerably in recent years, cardiovascular events remain one of the leading causes of death in people with SLE. Accelerated atherosclerosis in SLE is attributed both to an increase in traditional cardiovascular risk factors and the inflammatory effects of SLE itself. Many of these changes occur within the microenvironment of the vascular-immune interface, the site of atherosclerotic plaque development. Here, an intimate interaction between endothelial cells, vascular smooth muscle cells, and immune cells, dictates physiological versus pathological responses to a chronic type 1 interferon environment. Low-density neutrophils (LDNs) have also been implicated in eliciting vasculature-damaging effects at such lesion sites. These changes are thought to be governed by dysfunctional metabolism of immune cells in this niche due, at least in part, to the chronic induction of type 1 interferons. Understanding of these novel pathophysiological mechanisms and metabolic pathways may unveil potential innovative pharmacological targets and therapeutic opportunities for atherosclerosis, as well as shed light on the development of premature atherosclerosis in SLE patients who develop cardiovascular events.

中文翻译:

免疫代谢失调与血管损伤之间的联系:对系统性红斑狼疮和其他风湿性疾病中动脉粥样硬化发展的影响。

系统性红斑狼疮 (SLE) 的死亡率存在双峰模式。早期死亡主要由感染引起,而晚期死亡主要由动脉粥样硬化性疾病引起。此外,虽然近年来与 SLE 相关的死亡率大幅下降,但心血管事件仍然是 SLE 患者死亡的主要原因之一。SLE 中动脉粥样硬化的加速归因于传统心血管危险因素的增加和 SLE 本身的炎症效应。其中许多变化发生在血管-免疫界面的微环境内,即动脉粥样硬化斑块形成的部位。在这里,内皮细胞、血管平滑肌细胞和免疫细胞之间的密切相互作用决定了对慢性 1 型干扰素环境的生理反应和病理反应。低密度中性粒细胞(LDN)也与在此类病变部位引发脉管系统损伤作用有关。这些变化被认为是由该生态位中免疫细胞的代谢功能障碍所控制,至少部分是由于 1 型干扰素的长期诱导。了解这些新的病理生理机制和代谢途径可能会揭示动脉粥样硬化的潜在创新药理学靶点和治疗机会,并揭示发生心血管事件的 SLE 患者过早动脉粥样硬化的发展。
更新日期:2024-01-15
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