S C Bergkamp, M J Wahadat, A Salah, T W Kuijpers, V Smith, S W Tas, J M van den Berg, S Kamphuis, D Schonenberg-Meinema
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引用次数: 4
Abstract
Objectives: To perform a systematic literature review and meta-analysis on endothelial cell (EC) markers that are involved and dysregulated in systemic lupus erythematosus (SLE) in relation to disease activity, as EC dysregulation plays a major role in the development of premature atherosclerosis in SLE.
Methods: Search terms were entered into Embase, MEDLINE, Web of Science, Google Scholar and Cochrane. Inclusion criteria were 1) studies published after 2000 reporting measurements of EC markers in serum and/or plasma of SLE patients (diagnosed according to ACR/SLICC criteria), 2) English language peer reviewed articles, and 3) disease activity measurement. For meta-analysis calculations, the Meta-Essentials tool by Erasmus Research Institute and of Management (ERIM) was used. Only those EC markers, which were 1) reported in at least two articles and 2) reported a correlation coefficient (i.e. Spearman's rank or Pearson's) between the measured levels of the EC marker and disease activity were included. For meta-analyses, a fixed effect model was used.
Results: From 2133 hits, 123 eligible articles were selected. The identified SLE-related endothelial markers were involved in EC activation, EC apoptosis, disturbed angiogenesis, defective vascular tone control, immune dysregulation and coagulopathy. Meta-analyses of primarily cross-sectional studies showed significant associations between marker levels and disease activity for the following endothelial markers: Pentraxin-3, Thrombomodulin, VEGF, VCAM-1, ICAM-1, IP-10 and MCP-1. Dysregulated EC markers without associations with disease activity were: Angiopoeitin-2, vWF, P-Selectin, TWEAK and E-Selectin.
Conclusions: We provide a complete literature overview for dysregulated EC markers in SLE comprising a wide range of different EC functions. SLE-induced EC marker dysregulation was seen with, but also without, association with disease activity. This study provides some clarity in the eminent complex field of EC markers as biomarkers for SLE. Longitudinal data on EC markers in SLE are now needed to guide us more in unravelling the pathophysiology of premature atherosclerosis and cardiovascular events in SLE patients.
目的:对系统性红斑狼疮(SLE)中与疾病活动性相关的内皮细胞(EC)标志物进行系统的文献回顾和荟萃分析，因为内皮细胞(EC)的失调在SLE的过早动脉粥样硬化的发展中起着重要作用。方法:在Embase、MEDLINE、Web of Science、Google Scholar和Cochrane中输入检索词。纳入标准为:1)2000年以后发表的报告SLE患者(根据ACR/SLICC标准诊断)血清和/或血浆中EC标记物测量的研究;2)英文同行评议文章;3)疾病活动性测量。meta分析计算采用Erasmus Research Institute and of Management (ERIM)的Meta-Essentials工具。仅包括1)在至少两篇文章中报道的EC标记物，以及2)在EC标记物的测量水平与疾病活动性之间报告了相关系数(即Spearman's rank或Pearson's)。meta分析采用固定效应模型。结果:从2133次点击中，筛选出123篇符合条件的文章。所鉴定的slee相关内皮标志物参与EC激活、EC凋亡、血管生成紊乱、血管张力控制缺陷、免疫失调和凝血功能障碍。主要横断面研究的荟萃分析显示，以下内皮标志物的标志物水平与疾病活动性之间存在显著关联:penttraxin -3、血栓调节素、VEGF、VCAM-1、ICAM-1、IP-10和MCP-1。与疾病活动无关的失调EC标志物有:血管生成素-2、vWF、p -选择素、TWEAK和e -选择素。结论:我们提供了一个完整的文献综述失调的EC标记在SLE包括广泛的不同的EC功能。sled诱导的EC标记物失调与疾病活动性有关联，但也无关联。这项研究为EC标记物作为SLE生物标记物的复杂领域提供了一些清晰的信息。现在需要SLE中EC标记物的纵向数据来指导我们更多地揭示SLE患者早期动脉粥样硬化和心血管事件的病理生理学。
期刊介绍：
Journal of Inflammation welcomes research submissions on all aspects of inflammation.
The five classical symptoms of inflammation, namely redness (rubor), swelling (tumour), heat (calor), pain (dolor) and loss of function (functio laesa), are only part of the story. The term inflammation is taken to include the full range of underlying cellular and molecular mechanisms involved, not only in the production of the inflammatory responses but, more importantly in clinical terms, in the healing process as well. Thus the journal covers molecular, cellular, animal and clinical studies, and related aspects of pharmacology, such as anti-inflammatory drug development, trials and therapeutic developments. It also considers publication of negative findings.
Journal of Inflammation aims to become the leading online journal on inflammation and, as online journals replace printed ones over the next decade, the main open access inflammation journal. Open access guarantees a larger audience, and thus impact, than any restricted access equivalent, and increasingly so, as the escalating costs of printed journals puts them outside University budgets. The unrestricted access to research findings in inflammation aids in promoting dynamic and productive dialogue between industrial and academic members of the inflammation research community, which plays such an important part in the development of future generations of anti-inflammatory therapies.
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