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血清赖氨氧化酶样蛋白2(LOXL2)在冠状动脉疾病患者中升高且是独立生物标志物。

Serum LOXL2 is Elevated and an Independent Biomarker in Patients with Coronary Artery Disease.

作者信息

Zhu Zhongsheng

机构信息

Department of Cardiology, Guangming Traditional Chinese Medicine Hospital of Pudong New Area, Shanghai, 201321, People's Republic of China.

Department of Cardiology, Shanghai Pudong Hospital Affiliated to Fudan University, Shanghai, 201300, People's Republic of China.

出版信息

Int J Gen Med. 2024 Sep 14;17:4071-4080. doi: 10.2147/IJGM.S478044. eCollection 2024.

DOI:10.2147/IJGM.S478044
PMID:39295855
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11409929/
Abstract

BACKGROUND

Arterial stiffness is associated with accelerated progression of atherosclerosis and plaque rupture. Lysyl oxidase-like 2 (LOXL2) plays a vital role in inflammatory responses, matrix deposition and arterial stiffness. This study assessed the correlation between the serum LOXL2 concentration and disease severity, inflammation, and endothelial dysfunction of coronary artery disease (CAD).

METHODS

The study included 143 CAD patients and 150 non-CAD patients who underwent coronary angiography. Medical records, demographic and clinical baseline parameters were collected. Serum LOXL2 levels were measured using an ELISA kit.

RESULTS

CAD patients had higher serum LOXL2 levels than non-CAD patients, and LOXL2 levels were associated with severity of coronary lesions. Serum LOXL2 level was positively correlated with low-density lipoprotein cholesterol (LDL-C) (r=0.161, P=0.054), systolic blood pressure (SBP) (r=0.175, P=0.036), high-sensitivity C-reactive protein (hs-CRP) (r=0.177, P=0.035), intima-media thickness (IMT) (r=0.190, P=0.023), and brachial-ankle pulse wave velocity (baPWV) (r=0.203, P=0.015), while negatively associated with high-density lipoprotein cholesterol (HDL-C) (r=-0.191, P=0.023) and flow-mediated dilation (FMD) (r=-0.183, P=0.028) in CAD patients. Multivariate logistic regression showed that LOXL2 is independently correlated with LDL-C (OR=3.380; 95% CI=1.258-9.082; P=0.016), hs-CRP (OR=10.988; 95% CI=1.962-61.532; P=0.006), TC (OR=2.229; 95% CI=1.005-4.944; P=0.049), IMT (OR=72.719; 95% CI=2.313-2286.008; P=0.015), and baPWV (OR=1.002; 95% CI=1.001-1.004; P=0.005) in CAD patients. The receiver operating characteristic (ROC) curve showed that the best cut-off for CAD as serum LOXL2 is 275.35 pg/mL, with sensitivity and specificity of 77.6% and 84%, respectively.

CONCLUSION

Our data demonstrated that LOXL2 could be a potential biomarker and independent risk factor for CAD patients.

摘要

背景

动脉僵硬度与动脉粥样硬化的加速进展和斑块破裂相关。赖氨酰氧化酶样2(LOXL2)在炎症反应、基质沉积和动脉僵硬度中起重要作用。本研究评估了血清LOXL2浓度与冠状动脉疾病(CAD)的疾病严重程度、炎症及内皮功能障碍之间的相关性。

方法

该研究纳入了143例接受冠状动脉造影的CAD患者和150例非CAD患者。收集病历、人口统计学和临床基线参数。使用酶联免疫吸附测定(ELISA)试剂盒测量血清LOXL2水平。

结果

CAD患者的血清LOXL2水平高于非CAD患者,且LOXL2水平与冠状动脉病变的严重程度相关。血清LOXL2水平与CAD患者的低密度脂蛋白胆固醇(LDL-C)(r = 0.161,P = 0.054)、收缩压(SBP)(r = 0.175,P = 0.036)、高敏C反应蛋白(hs-CRP)(r = 0.177,P = 0.035)、内膜中层厚度(IMT)(r = 0.190,P = 0.023)和臂踝脉搏波速度(baPWV)(r = 0.203,P = 0.015)呈正相关,而与高密度脂蛋白胆固醇(HDL-C)(r = -0.191,P = 0.023)和血流介导的血管舒张(FMD)(r = -0.183,P = 0.028)呈负相关。多因素逻辑回归显示,在CAD患者中,LOXL2与LDL-C(比值比[OR]=3.380;95%置信区间[CI]=1.258 - 9.082;P = 0.016)、hs-CRP(OR = 10.988;95% CI = 1.962 - 61.532;P = 0.006)、总胆固醇(TC)(OR = 2.229;95% CI = 1.005 - 4.944;P = 0.049)、IMT(OR = 72.719;95% CI = 2.313 - 2286.(此处原文有误,推测应为2286.008)08;P = 0.015)和baPWV(OR = 1.002;95% CI = 1.001 - 1.004;P = 0.005)独立相关。受试者工作特征(ROC)曲线显示,CAD的血清LOXL2最佳截断值为275.35 pg/mL,敏感性和特异性分别为77.6%和84%。

结论

我们的数据表明,LOXL2可能是CAD患者的潜在生物标志物和独立危险因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9f6/11409929/0d51df3027cf/IJGM-17-4071-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9f6/11409929/80cfa522e303/IJGM-17-4071-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9f6/11409929/1a884207edf1/IJGM-17-4071-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9f6/11409929/0abcd73ff0c0/IJGM-17-4071-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9f6/11409929/0d51df3027cf/IJGM-17-4071-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9f6/11409929/80cfa522e303/IJGM-17-4071-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9f6/11409929/1a884207edf1/IJGM-17-4071-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9f6/11409929/0abcd73ff0c0/IJGM-17-4071-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c9f6/11409929/0d51df3027cf/IJGM-17-4071-g0004.jpg

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