• Yu-Wei Liu, Qun-Fang Yang, Pei-Yuan Zuo, Chang-Liang Xiao, Xing-Lin Chen, and Cheng-Yun Liu.
• Departments of Geriatrics, and Hyperbaric Oxygen Center, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, P.R. China.
• Am. J. Med. Sci. 2015 Feb 1; 349 (2): 124129124-9.

BackgroundMorbidities related to atherosclerosis, such as acute coronary syndrome (ACS), remain the leading cause of mortality. Axl is a receptor tyrosine kinase that is expressed in mammalian vascular and immune cells. Axl signaling is involved in the regulation of the inflammatory response. A considerable amount of evidence indicates that inflammation is responsible for the development of atherosclerosis in patients with ACS.MethodsTo assess the relation of Axl and ACS, we recruited 64 patients with coronary heart disease: 34 with ACS, 30 with stable coronary heart disease, and 24 apparently healthy controls. Serum concentrations of soluble Axl (sAxl) were quantified by enzyme-linked immunosorbent assay. High-sensitivity C-reactive protein, tumor necrosis factor alpha, troponin I, and other routine biochemical markers were also measured.ResultsThe levels of sAxl were significantly higher in patients with ACS than in the controls (P=0.005). Furthermore, correlation analysis indicated that sAxl was significantly associated with serum levels of high-sensitivity C-reactive protein (r=0.283, P=0.008), tumor necrosis factor alpha (r=0.565, P<0.001), and troponin I (r=0.264, P=0.013). Logistic regression analysis (odds ratio=1.038, 95% confidence interval, 1.008-1.069, P=0.012) indicated a significant association between sAxl and ACS.ConclusionsSerum levels of sAxl correlate to inflammatory biochemical markers. These findings demonstrate for the first time that sAxl does have a role in ACS, presumably connected to the inflammation.

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