Systemic Inflammatory Response and Atherosclerosis: The Paradigm of Chronic Inflammatory Rheumatic Diseases.
Systemic Inflammatory Response and Atherosclerosis: The Paradigm of Chronic Inflammatory Rheumatic Diseases.
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DOI：
10.3390/ijms19071890
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发表时间：
2018-06-27
影响因子：
5.6
通讯作者：
Sfikakis PP
中科院分区：
文献类型：
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作者：
Arida A;Protogerou AD;Kitas GD;Sfikakis PP
慢性炎症性风湿病（CIRD）患者患心血管疾病（CVD）的风险增加，这不仅归因于经典危险因素，还归因于慢性全身炎症反应的存在。众所周知，动脉粥样硬化是 CVD 的基石，在 CIRD 中会加速；类风湿性关节炎会促进动脉粥样硬化，并与相当于糖尿病的临床前动脉粥样硬化相关，这似乎也适用于系统性红斑狼疮。关于强直性脊柱炎和银屑病关节炎的数据虽然较为有限，但也支持这些患者的心血管风险增加。炎症与动脉粥样硬化之间的关联在过去三十年中已得到彻底研究，并且炎症在动脉粥样硬化的发病机制和进展中的作用已得到充分确定。内皮功能障碍、血管内皮细胞和巨噬细胞的氧化应激、Toll 样受体信号传导、NLPR-3 的形成以及随后的促炎细胞因子的产生，如 TNFa、IL-1β、IL-6 和 TNF 样细胞因子 1A，是与动脉粥样硬化过程有关的少数机制。此外，有证据表明，抗炎生物药物，如抗TNF和抗IL1β药物，可以减缓动脉粥样硬化过程，从而除了积极管理经典心血管危险因素外，还可以为早期有效的疾病控制和抑制炎症设定新的治疗目标。
Patients with Chronic Inflammatory Rheumatic diseases (CIRD) are at increased risk of cardiovascular disease (CVD), ascribed not only to classical risk factors, but also to the presence of chronic systemic inflammatory response. Αtherosclerosis, the cornerstone of CVD, is known to be accelerated in CIRD; rheumatoid arthritis promotes atheromatosis and associates with preclinical atherosclerosis equivalent to Diabetes Mellitus, which also seems to apply for systemic lupus erythematosus. Data on ankylosing spondylitis and psoriatic arthritis, albeit more limited, also support an increased CV risk in these patients. The association between inflammation and atherosclerosis, has been thoroughly investigated in the last three decades and the role of inflammation in the pathogenesis and progression of atherogenesis has been well established. Endothelial dysfunction, oxidative stress in vascular endothelial cells and macrophage accumulation, toll-like receptor signaling, NLPR-3 formation and subsequent pro-inflammatory cytokine production, such as TNFa, IL-1β, IL-6, and TNF-like cytokine 1A, are few of the mechanisms implicated in the atherogenic process. Moreover, there is evidence that anti-inflammatory biologic drugs, such as anti-TNF and anti-IL1β agents, can decelerate the atherogenic process, thus setting new therapeutic targets for early and effective disease control and suppression of inflammation, in addition to aggressive management of classical CV risk factors.
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