title: Association of four genetic polymorphisms of AGER and its circulating forms with coronary artery disease: a meta-analysis.
abstract: BACKGROUND
  Considerable efforts have been devoted to evaluating the association of the receptor for advanced glycation end-products (gene AGER and protein: RAGE) genetic variants to coronary artery disease (CAD); the results, however, are often irreproducible. To generate more information, we sought to explore four common polymorphisms of AGER and its circulating forms associated with the risk of CAD via a meta-analysis.
  
  
  RESULTS
  Articles were identified by searching PubMed, EMBASE, Wanfang and CNKI databases before March 2013. Qualified articles had case-control designs and investigated AGER four polymorphisms (T-429C, T-374A, Gly82Ser, G1704A) or circulating soluble RAGE (sRAGE) or endogenous secretory RAGE (esRAGE) levels associated with CAD. Twenty-seven articles involving 39 independent groups fulfilled the predefined criteria. Overall, no significance was observed for all examined polymorphisms under allelic and dominant models. When restricting groups to CAD patients with diabetes mellitus or renal disease, deviations of risk estimates from the unity were stronger than overall estimates for all polymorphisms except for G1704A due to limited available studies. For example, under dominant model, having -429C allele increased the odds of developing CAD in diabetic patients by 1.22-fold (95% confidence interval (95% CI) 0.99-1.51; P = 0.06; I (2) = 6.7%) compared with that of overall estimate of 1.15-fold (95% CI: 0.97-1.36; P = 0.111; I (2) = 18.0%). Circulating sRAGE levels were non-significantly lower in CAD patients than in controls, whereas this reduction was totally and significantly reversed in CAD patients with diabetes mellitus (weighted mean difference: 185.71 pg/ml; 95% CI: 106.82 to 264.61 pg/ml). Circulating esRAGE levels were remarkably lower in CAD patients, as well as in subgroups with or without diabetes mellitus and without renal disease.
  
  
  CONCLUSIONS
  Our findings demonstrated that association of AGER genetic polymorphisms with CAD was potentiated in patients with diabetes mellitus or renal disease. Practically, circulating esRAGE might be a powerful negative predictor for the development of CAD.
authors.affiliation: Department of Cardiology, the First Affiliated Hospital of Fujian Medical University, Fuzhou, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Peng
authors.forename: Dan
authors.initials: D
authors.lastname: Hu
authors.forename: Nan
authors.initials: N
authors.lastname: Jia
authors.forename: Xiaobo
authors.initials: X
authors.lastname: Li
authors.forename: Yuqiong
authors.initials: Y
authors.lastname: Li
authors.forename: Shaoli
authors.initials: S
authors.lastname: Chu
authors.forename: Dingliang
authors.initials: D
authors.lastname: Zhu
authors.forename: Weifeng
authors.initials: W
authors.lastname: Shen
authors.forename: Jinxiu
authors.initials: J
authors.lastname: Lin
authors.forename: Wenquan
authors.initials: W
authors.lastname: Niu
mesh_terms: D003324:Coronary Artery Disease / Q000235:genetics*; D017127:Glycation End Products, Advanced / Q000235:genetics*; D006801:Humans; D011110:Polymorphism, Genetic; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000235:genetics*; D012307:Risk Factors
chemical_list: D017127:Glycation End Products, Advanced; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic
references.citation: Int J Mol Med. 2004 Dec;14(6):1061-4
references.pmid: 15547674
references.citation: PLoS One. 2012;7(12):e50790
references.pmid: 23236395
references.citation: Curr Mol Med. 2007 Dec;7(8):699-710
references.pmid: 18331228
references.citation: Diabetes. 2001 Jun;50(6):1505-11
references.pmid: 11375354
references.citation: Atherosclerosis. 2009 Aug;205(2):544-8
references.pmid: 19150066
references.citation: Mol Med. 2007 Nov-Dec;13(11-12):625-35
references.pmid: 17932553
references.citation: Circ J. 2011;75(7):1685-90
references.pmid: 21576827
references.citation: Coron Artery Dis. 2007 Feb;18(1):1-8
references.pmid: 17172923
references.citation: Atherosclerosis. 2005 Oct;182(2):301-5
references.pmid: 16159602
references.citation: Atherosclerosis. 2009 Dec;207(2):597-602
references.pmid: 19576587
references.citation: In Vivo. 2009 Nov-Dec;23(6):949-54
references.pmid: 20023238
references.citation: J Am Soc Nephrol. 2004 Jul;15(7):1889-96
references.pmid: 15213278
references.citation: Stroke. 2006 Jul;37(7):1686-90
references.pmid: 16728681
references.citation: Coll Antropol. 2004 Dec;28(2):611-6
references.pmid: 15666591
references.citation: Atherosclerosis. 2011 Aug;217(2):536-42
references.pmid: 21663912
references.citation: Rejuvenation Res. 2011 Feb;14(1):67-73
references.pmid: 21208063
references.citation: Mol Genet Metab. 2005 Jun;85(2):149-56
references.pmid: 15896660
references.citation: J Renin Angiotensin Aldosterone Syst. 2013 Mar;14(1):82-90
references.pmid: 22782431
references.citation: Genet Test Mol Biomarkers. 2012 Feb;16(2):134-7
references.pmid: 21861709
references.citation: Arch Intern Med. 2008 May 26;168(10):1077-89
references.pmid: 18504336
references.citation: Ann Intern Med. 2009 Aug 18;151(4):264-9, W64
references.pmid: 19622511
references.citation: Arch Med Res. 2009 Jul;40(5):393-8
references.pmid: 19766904
references.citation: BMC Med Res Methodol. 2011 Apr 07;11:41
references.pmid: 21473747
references.citation: Heart. 2012 Oct;98(20):1483-91
references.pmid: 22689717
references.citation: J Hum Genet. 2010 Oct;55(10):668-75
references.pmid: 20668462
references.citation: Expert Opin Investig Drugs. 2008 Jul;17(7):983-96
references.pmid: 18549336
references.citation: Clin Chim Acta. 2008 Oct;396(1-2):33-7
references.pmid: 18638464
references.citation: Mol Cell Endocrinol. 2012 Jul 6;358(1):9-17
references.pmid: 22402134
references.citation: Atherosclerosis. 2009 Oct;206(2):540-5
references.pmid: 19368923
references.citation: Crit Care Med. 2012 May;40(5):1513-22
references.pmid: 22430238
references.citation: Diabetes Technol Ther. 2012 Oct;14(10):936-42
references.pmid: 22856651
references.citation: Atherosclerosis. 2008 Mar;197(1):217-23
references.pmid: 17499742
references.citation: Clin Cardiol. 2010 Nov;33(11):678-85
references.pmid: 21089112
references.citation: Mol Cell Biochem. 2010 Aug;341(1-2):135-8
references.pmid: 20339904
references.citation: Cardiovasc Diabetol. 2011 May 18;10:41
references.pmid: 21592353
references.citation: World J Cardiol. 2012 Apr 26;4(4):90-102
references.pmid: 22558488
references.citation: Arterioscler Thromb Vasc Biol. 2005 May;25(5):1032-7
references.pmid: 15731496
references.citation: Atherosclerosis. 2009 May;204(1):288-92
references.pmid: 18926539
references.citation: Circulation. 2002 Nov 26;106(22):2827-35
references.pmid: 12451010
references.citation: Microvasc Res. 2008 May;76(1):52-6
references.pmid: 18474381
references.citation: Am J Kidney Dis. 2006 Mar;47(3):406-11
references.pmid: 16490618
references.citation: Int J Cardiol. 2012 May 31;157(2):243-52
references.pmid: 22261689