We reported the relationship between plasma TK levels and severity of CAD in the present study. The severity of CAD was evaluated using vessel scores and stenosis scores. It is interesting to note that plasma TK levels were negatively associated with the severity of CAD according to vessel and stenosis scores. These results suggest that decreased plasma TK levels might predict the severity of CAD. Numerous studies have demonstrated that TK inhibits the proliferation of cultured vascular smooth muscle cells and neointimal formation in blood vessels after balloon angioplasty stimulate endothelial cell proliferation, attenuate vascular injury by promoting vascular regeneration and accelerating spontaneous angiogenesis. Taken together, these indicate that TK may have significant implications for protecting against atherosclerosis and ischemic vascular disease and may be a prognostic tool for evaluating the extent of obstructive CAD. Overexpression of the human TK gene in spontaneously hypertensive rats induced hypotension, and epidemiological studies, which are consistent with our findings regarding the negative association between plasma TK levels and a history of hypertension in controls. Our finding showed that plasma TK levels had an inverse SJN 2511 446859-33-2 correlation with a history of hyperlipidemia as well. These data suggest that plasma TK may influence blood pressure and lipid metabolism. Further prospective and basic studies are still needed to elucidate the role of TK on lipid metabolism. In addition, our previous study demonstrated that plasma TK level was negatively associated with the risk of first-ever stroke and stroke recurrence. As plasma TK levels were increased in diabetes and CAD, decreased plasma TK levels might be specific biomarker in stroke. Our study has several limitations. First, the case-control design limited our ability to establish a causal link between elevated plasma TK levels and CAD. As a result, the relationship between plasma TK level and the risk of CAD should be verified in future prospective studies. Second, even though the multivariate analysis adjusted for the traditional risk factors, it is still possible that the confounding elements cannot be “adjusted out”. Third, it was impossible to avoid the influence of medications on plasma TK levels completely, although the associations of drugs with plasma TK levels were not apparent in previous studies. Fourth, the relationship between plasma TK level and timing for the progression of cardiovascular disease might be an important evidence to indicate that TK plays an important role associated with CAD. These questions can only be addressed through additional prospective studies of the association of TK with firstever CAD and the extent of obstructive CAD. In conclusion, our research, combined with previous basic studies, suggest that elevated TK is positively associated with the presence of CAD and negatively associated with the severity of CAD and that they might be a strong and independent biomarker of CAD in the Chinese population.