Association between new circulating proinflammatory and anti-inflammatory adipocytokines with coronary artery disease

新发现的循环促炎和抗炎脂肪细胞因子与冠状动脉疾病之间的关联

阅读:2

Abstract

BACKGROUND: The aim of this study was to evaluate the diagnostic and risk predictive value of emerging proinflammatory and anti-inflammatory adipocytokines on coronary artery disease (CAD). PATIENTS AND METHODS: The study involved 259 inpatients suspected acute coronary syndrome who underwent coronary angiography. Demographic, clinical characteristics, and coronary artery stenosis rated by Gensini score were collected by cardiovascular doctors. The levels of serum inflammatory adipocytokines were evaluated by ELISA. The correlations of the cytokines with clinical parameters were assessed. Receiver operating characteristic curves were constructed for the diagnosis of CAD. RESULTS: The 259 inpatients were assigned to the CAD (n = 180) and control groups (n = 79). Compared with the control group, the CAD group displayed significantly higher serum levels of retinol-binding protein-4 (RBP4), pentraxin 3 (PTX3), galectin-3 (GAL-3), and plasminogen activator inhibitor (PAI-1), and significantly lower levels of netrin-1 (NTN1), interleukin-37 (IL-37), and adiponectin (ADP) (all P < 0.05). PAI-1 was significantly upregulated, and IL-37 and ADP were significantly downregulated in the three-vessels CAD subgroup compared to the one- and two-vessels CAD subgroups (P < 0.05). The RBP4, PTX3, GAL-3, PAI-1, and IL-37 inflammatory cytokines were significantly positively correlated with Gensini score, and ADP was negatively correlated (all P < 0.001). IL-37 was a more accurate anti-inflammatory biomarker than NTN1 and ADP. Combining cytokines significantly increased the sensitivity and specificity. CONCLUSION: The inflammatory adipocytokines GAL-3, RBP4, PTX3, NTN1, and IL-37 were more effective than the classical biomarkers PAI-1 and ADP in the diagnosis and risk assessment of CAD patients.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。