title: Does adenosine deaminase play a key role in coronary artery disease.
abstract: Adenosine deaminase (ADA) is an enzyme which catalyzes adenosine to inosine. Patients who inherently lack the enzyme have defects in both humoral and cellular immunity. ADA plays an important role in many immunity mediate diseases, such as asthma, Graves' disease and tuberculosis. Coronary artery disease (CAD) has been considered as an inflammatory and immunizing disease recently. However, there are few reports about the effect of ADA in cardiovascular fields. In fact, ADA may play a key role in the immunity, inflammation and other aspects of CAD. This hypothesis is potentially based on three aspects of evolution. First, ADA inhibitors attenuate the elevation of proinflammatory factors, which shows ADA mediate in the inflammation response. ADA also has effect on the activation of complement system by the deamination of adenosine. Thus, ADA has a role in CAD by affecting inflammation process. Second, many effects produced by ADA are caused by the metabolism of adenosine. It is known that adenosine can inhibit the invasion of the neutrophil so as to attenuate the ischemic/reperfusion injury . Adenosine can increase coronary artery blood flow during active stress and hypoxia to balance the oxygen supply and demand. Adenosine can also account for the majority of basal vascular endothelial growth factor (VEGF) mRNA and protein expression in cultured myocardial vascular smooth muscle cells under normoxic conditions to stimulate the angiogenesis. If adenosine is rapidly metabolized by the high level of ADA, the advantages of adenosine will lost. Finally, adenosine is catalyzed to inosine, which can produce superoxide radicals and exaggerate the ischemic/reperfusion injury. In conclusion ADA can have a crucial role in CAD, if design and development of therapeutic strategies against ADA is guaranteed, an innovational therapeutic approach to CAD can be realized.
authors.affiliation: Department of Cardiology, Beijing AnZhen Hospital, Capital University of Medical Sciences, Chaoyang District, Beijing 100029, China. tangribo1994@yahoo.com.cn
authors.forename: RiBo
authors.initials: R
authors.lastname: Tang
authors.forename: ChangSheng
authors.initials: C
authors.lastname: Ma
authors.forename: JianZeng
authors.initials: J
authors.lastname: Dong
authors.forename: XingPeng
authors.initials: X
authors.lastname: Liu
authors.forename: Xiaohui
authors.initials: X
authors.lastname: Liu
mesh_terms: D000243:Adenosine Deaminase / Q000502:physiology*; D058892:Adenosine Deaminase Inhibitors; D003324:Coronary Artery Disease / Q000188:drug therapy / Q000201:enzymology* / Q000628:therapy; D004791:Enzyme Inhibitors / Q000627:therapeutic use; D005609:Free Radicals / Q000378:metabolism; D015316:Genetic Therapy; D006801:Humans; D013481:Superoxides / Q000378:metabolism
chemical_list: D058892:Adenosine Deaminase Inhibitors; D004791:Enzyme Inhibitors; D005609:Free Radicals; D013481:Superoxides; D000243:Adenosine Deaminase