Increased circulating levels of tumor necrosis factor-like cytokine 1A and decoy receptor 3 correlate with SYNTAX score in patients undergoing coronary surgery

Abstract

Objective Chronic inflammation of the arteries is a critical mechanism responsible for coronary atherosclerosis. We aimed to determine if tumor necrosis factor (TNF)-like cytokine 1A (TL1A) and decoy receptor 3 (DcR3) were involved in promoting atherosclerosis. Methods We compared plasma levels of TL1A and DcR3 in patients with coronary artery disease (CAD) undergoing coronary artery bypass grafting (n=40) and patients without CAD group (n=37, normal coronary artery angiogram) by enzyme-linked immunosorbent assay. We also analyzed the correlation between CAD and SYNTAX scores. Results Plasma levels of TL1A and DcR3 were significantly higher in the CAD compared with the no-CAD group. Multivariate analysis showed that TL1A and DcR3 were significantly correlated with the presence of CAD, and receiver operating characteristic curve analysis indicated that both TL1A and DcR3 showed high sensitivity and specificity for diagnosing CAD. Furthermore, TL1A was positively and significantly correlated with SYNTAX score in CAD patients. Conclusions CAD patients requiring coronary artery bypass grafting have high circulating levels of both TL1A and DcR3, which may thus be useful biomarkers for diagnosing severe CAD. Furthermore, plasma levels of TL1A correlate with SYNTAX score, supporting its potential use as an indicator of the severity of CAD.

Soluble Tumor Necrosis Factor Receptor 1 is Associated With Cardiovascular Risk in Persons With Coronary Artery Calcium Score of Zero

“…They are useful markers of TNF-α activity due to their long half-lives in the serum. TNF-α has been linked to increased cardiovascular events in a 5-year period post myocardial infarction [ 8 ] as well as CAD complexity [ 9 ]. Several TNF-alpha blockers are approved for use in patients with chronic inflammatory conditions, such as rheumatoid arthritis and inflammatory bowel disease.…”

Research Progress of DcR3 in the Diagnosis and Treatment of Sepsis

“…The physiological role of DcR3 is not fully understood, but as a soluble receptor in the decoy receptor family, DcR3 can neutralize the biological effects of FasL, LIGHT, and TL1A through its decoy function [ 24 ]. As shown in Figure 2 , DcR3 can competitively bind these ligands due to higher affinity, blocking downstream signaling and exerting anti-apoptotic and anti-inflammatory effects by reducing the original biological activity of the ligand [ 12 , 25 , 26 , 27 ]. Furthermore, DcR3 exerts a non-decoy function through acetyl heparan sulfate proteoglycan (HSPG), which can regulate macrophage differentiation toward the M2 type, regulate the T-helper 1/2 cells (Th1/Th2) bias toward Th2 differentiation, and promote monocyte cell adhesion [ 28 ].…”

Decoy Technology as a Promising Therapeutic Tool for Atherosclerosis

“…Tumor necrosis factor (TNF)-like cytokine 1A (TL1A), which belongs to the TNF superfamily, plays critical roles in the development of chronic inflammation [ 82 ]. TL1A receptors include decoy receptor 3 (DcR3), and death receptor 3 belongs to the TNF receptor superfamily [ 83 ].…”

“…Moreover, it was shown that DcR3 and TL1A have high specificity and sensitivity for diagnosis of CAD with TL1A being positively and significantly correlated with the Syntax score in CAD patients. The circulating levels of both TL1A and DcR3 were higher in CAD patients and required more coronary artery bypass grafting than in the control subjects, thus making them potential biomarkers for diagnosing severe CAD [ 83 ].…”