Abstract
This study aimed to investigate the associations of circulating long, non-coding (lncRNA) IFNG-AS1, lncRNA ANRIL and lncRNA ITSN1 relative expressions with disease risk, severity and inflammatory cytokines levels in coronary artery disease (CAD) patients. One hundred and ninety-one patients suspected of CAD who underwent coronary angiography were consecutively enrolled in this casecontrol study, and divided into CAD patients (N=102) and controls (N=89) according to coronary angiographic results. Blood samples of all participants were collected. Plasma lncRNA IFNG-AS1, lncRNA ANRIL and lncRNA ITSN1 expressions were detected using quantitative polymerase chain reaction (qPCR). Serum tumor necrosis factor-α (TNF-α), interleukin (IL)-1β (IL-1β), IL-6, IL-8, IL-10, and IL-17 were assessed using enzyme-linked immunosorbent assay (ELISA). Gensini Score was used to evaluate the disease severity of CAD patients. LncRNA IFNG-AS1 relative expression in CAD patients was upregulated compared with that in controls (P<.001), and the receiver operating characteristic (ROC) curve showed that the area under curve (AUC) of lncRNA-IFNG-AS1 for predicting the risk of CAD was 0.755 (95% CI: 0.688-0.821). lncRNA IFNG-AS1 relative expression was remarkably associated with Gensini Score (r=.259, P=.009). Additionally, lncRNA IFNG-AS1 relative expression was positively associated with high-sensitivity C-reactive protein (hs-CRP) (r=.283, P=.004), TNF-α (r=.269, P=.006), and IL-6 levels (r=.425, P<.001), while it was negatively correlated with IL-10 level (r=-.263, P=.008). lncRNA ANRIL or lncRNA ITSN1 was not correlated with CA D risk, Gensini Score, hs-CRP, ESR, TNF-α, IL-1β, IL-6, IL-8, IL-10, or IL-17 levels (all P>.05). Circulating lncRNA IFNG-AS1 expression correlates with increased disease risk, higher disease severity and elevated inflammation in CAD patients.
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.
