Abstract
Increasing evidences suggest that inflammation plays an important role in the pathogenesis of coronary artery disease (CAD). Numerous inflammatory cytokines and related genes mediate adverse cardiovascular events in patients with CAD, such as interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and Homer in the present study. The study was carried out on 163 CAD patients at different stages and 68 controls. The gene expression of Homer1, Homer2, Homer3, IL-1β, and TNF-α in the peripheral blood leukocytes were measured by real-time polymerase chain reaction. The mRNA levels of Homer1, IL-1β, and TNF-α in CAD patients were significantly higher than those in the control group, but not Homer2 and Homer3. However, there was no considerable difference in the mRNA levels of Homer1, IL-1β, and TNF-α among AMI, UAP, and SAP three subgroups of CAD. The receiver operating characteristic (ROC) curves showed that Homer1 had a better diagnostic value for UAP patients compared with IL-1β and TNF-α. Like IL-1β and TNF-α, Homer1 may also be an important participant of atherosclerotic plaque development and eventually rupture. The results of the present study may provide an important basis for diagnosing CAD patients, and provide new therapeutic targets for CAD.
Highlights
Coronary artery disease (CAD) has become a public health problem with high morbidity and mortality worldwide, with an estimated more than 700,000 deaths annually in China [1,2]
We investigated the gene expression of Homer1, Homer2, Homer3, and pro-inflammatory cytokines, IL-1β and tumor necrosis factor-α (TNF-α) in the peripheral blood leukocytes, which may all relate to the inflammatory immune response
We demonstrated that the gene expression of Homer1, IL-1β and TNF-α in the peripheral blood leukocytes were associated with CAD, but not Homer2 and
Summary
Coronary artery disease (CAD) has become a public health problem with high morbidity and mortality worldwide, with an estimated more than 700,000 deaths annually in China [1,2]. Patients with CAD can present with stable angina pectoris (SAP), unstable angina pectoris (UAP), or acute myocardial infarction (AMI). Many studies showed that CAD is mainly caused by an interaction between genetic and environmental factors [3]. Increasing evidences suggest that inflammation plays an important role in the pathogenesis of both the chronic and acute phases of CAD [4,5,6]. The common cause of CAD is the formation of plaque and the rupture of the unstable atherosclerotic plaque. Recent molecular studies have shown altered mRNA level of many genes in both atherosclerotic plaque and peripheral blood cells may associate with CAD [7]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
